Genome complexity (Introduction)

by David Turell @, Monday, August 27, 2012, 16:12 (2220 days ago)

Obvously, discoveries to come will show that things will get more and more complex; why are those RNA's sleeping?

http://phys.org/news/2012-08-cap-scientists-rna-phenomenon-dogma.html

Genome complexity

by David Turell @, Wednesday, November 21, 2012, 15:02 (2134 days ago) @ David Turell

RNAzymes are non-coding RNA's that help with proper folding of newly made proteins.

http://phys.org/news/2012-11-rna-cooperation.html

Genome complexity

by David Turell @, Friday, November 30, 2012, 04:41 (2125 days ago) @ David Turell

Long non-coding RNa seems to have function, but what? We will find out as research progresses.

http://www.biocompare.com/Editorial-Articles/122205-Long-Non-coding-RNAs/

Epigenetics marches on. goodbye neo-Darwiism.

Genome complexity

by David Turell @, Sunday, December 09, 2012, 00:17 (2116 days ago) @ David Turell

it was obvious to me that the discovery of DNA and its coding for protein was just a tiny beginning of the complexity. We now have layers of codes upon codes and expression-of-genes systems galore. Just making protein doesn't tell us how the living cell really operates. Now in plants there are gene-expression non-transcription areas:


"Conserved noncoding sequences (CNSs) in DNA are reliable pointers to regulatory elements controlling gene expression. Using a comparative genomics approach with four dicotyledonous plant species (Arabidopsis thaliana, papaya [Carica papaya], poplar [Populus trichocarpa], and grape [Vitis vinifera]), we detected hundreds of CNSs upstream of Arabidopsis genes. Distinct positioning, length, and enrichment for transcription factor binding sites suggest these CNSs play a functional role in transcriptional regulation. The enrichment of transcription factors within the set of genes associated with CNS is consistent with the hypothesis that together they form part of a conserved transcriptional network whose function is to regulate other transcription factors and control development. We identified a set of promoters where regulatory mechanisms are likely to be shared between the model organism Arabidopsis and other dicots, providing areas of focus for further research."

http://www.plantcell.org/content/24/10/3949

And further commentary:

http://www2.warwick.ac.uk/newsandevents/pressreleases/discovery_of_100

The more complex, the less likely for chance, and the more likely a case for design.

Genome complexity

by hyjyljyj @, Sunday, December 09, 2012, 13:57 (2116 days ago) @ David Turell

David: "The more complex, the less likely for chance, and the more likely a case for design."

That really is it in a nutshell, isn't it?

The more complex, the greater the number of bizarre coincidences occurring with flawless precision in type, location, magnitude and timing that we are expected to believe in, rather than believing in what's staring us in the face.

If it were only ONE single, giant, heaving coincidence bringing about life on Earth, for example, we MIGHT -- I say MIGHT -- be persuaded that it was just happenstance. When an unimaginable number of them are required just to make a single protein, and then another unimaginable number of them to get to the next level of organization, then another and another, at some point we get to ask, Are you kidding? Like the universe is just dying to create this insane level of order from chaos, against the gradient of entropy? Really? Then I guess I'll dump this box of spaghetti out of a helicopter and watch the noodles all fall to earth and stand vertically atop each other, end to end, stretching up into the sky. If the chance thing is true, then I ought to be able to get that comparatively simple, straightforward result in a ridiculously short time; it's not like I'm looking for the spontaneous generation of the first protein molecule or echidna. So once I stack them perfectly on my first or second try, then I'll go back up on my next flight, dump out another box and watch them spell out God Save the Queen. Because to those fully invested in Holy Random Chance as the Guiding Influence of the universe, there is, by definition, NO chain of events so unlikely that it would take more than 13.5 billion years to happen along.

(Wonder how much fuel I'd burn on repeat flights, as the noodles kept messing up and misspelling it: God Shave the Queen, then God Save the Queer, then Rod Gave Me Beer, then...)

Genome complexity

by David Turell @, Sunday, December 09, 2012, 15:04 (2116 days ago) @ hyjyljyj

David: "The more complex, the less likely for chance, and the more likely a case for design."

hy: If it were only ONE single, giant, heaving coincidence bringing about life on Earth, for example, we MIGHT -- I say MIGHT -- be persuaded that it was just happenstance. When an unimaginable number of them are required just to make a single protein, and then another unimaginable number of them to get to the next level of organization, then another and another, at some point we get to ask, Are you kidding?

What I have always wondered is, did the Lords of Evolution, those University Ph.D.s ever take organic chemistry in college and then carry that knowledge over to look at the complexity of one organic enzyme made up of humdreds of amino acids, folded just so? And now finding that there are several layers of translation so that enzyme can be altered to do several jobs, not just one.

Darwin thought cells were simple blobs of protoplasm. I am quite sure Charlie would not have presented his theory so simply if he had the knowledge we have today. But you are right, it doesn't dissuade his stary-eyed atheist followers.

Genome complexity; another layer

by David Turell @, Tuesday, December 11, 2012, 16:11 (2114 days ago) @ David Turell

A new study on the ciradian cycles shows the epigenetic controls of the mouse liver:

"In the case of humans and other vertebrates, a brain structure called the suprachiasmatic nucleus controls circadian responses. But there are also clocks throughout the body, including our visceral organs, that tell specific genes when to make the workhorse proteins that enable basic functions in our bodies, such as producing glucose for energy. In the liver, genes that control the metabolism of fat and cholesterol turn on and off in sync with these clocks. But genes do not switch on and off by themselves. Their activity is regulated by the "epigenome," a set of molecules that signal to the genes how many proteins they should make, and, most importantly from the circadian point of view, when they should be made."

Read more at: http://medicalxpress.com/news/2012-12-epigenetic-daily-liver.html#jCp

Genome complexity; another layer

by David Turell @, Tuesday, December 11, 2012, 18:39 (2114 days ago) @ David Turell

More complexity:

http://www.genomeweb.com/arrays/copy-machines


"Such early CNV [copy number variations] work, though, generally presumed that such variants were rare, deleterious events, usually linked to disease. This understanding, Lee says, held until 2004, when a pair of papers — one by Lee and his collaborators in Nature Genetics and another in Science by Cold Spring Harbor Laboratory researcher Michael Wigler and colleagues — appeared a week apart, both demonstrating that CNVs were widespread throughout the human genome and likely a significant source of natural genetic variation.

"Prior to 2004, [copy number] gains and losses were thought to be very rare and associated with highly penetrant genomic disorders," Lee says. "It wasn't until 2004 [that] our group and the group of Mike Wigler published papers back to back showing that there are a lot of gains and losses in the human genome in healthy individuals."

And found in genetic diseases

Genome complexity; quick DNA repair

by David Turell @, Friday, December 14, 2012, 01:09 (2111 days ago) @ David Turell

Quick is necessary as mitosis is quick. More complexity, of course:

http://phys.org/news/2012-12-team-mystery-dna.html

Genome complexity;timing copies

by David Turell @, Saturday, December 29, 2012, 15:19 (2096 days ago) @ David Turell

When transcribing from DNA bits of the code are gradually stuck together, but thre is a pause before final instructions are given. That pause mechanism is now found:

http://darwins-god.blogspot.com/2012/12/here-is-how-genes-are-exquisitely-timed.html

Look at the graphical abstract:

http://www.cell.com/cell-reports/retrieve/pii/S2211124712004214?_returnURL=http://linki...

The complexity continues to build with each new discovery. God the designer, anyone!

Genome complexity; another code

by David Turell @, Monday, January 21, 2013, 14:53 (2073 days ago) @ David Turell

Varying production of amino acids under stress:

"What we found was that if the bacteria are in an environment where they can grow and thrive, each synonymous codon produces the same amount of protein," Subramaniam said. "But the moment we put them in an environment where they are starved of an amino acid, some codons produce a hundredfold more proteins than others." The difference, he said, lay with molecules called transfer RNA, or tRNA, which ferry amino acids to the cellular machinery that manufactures proteins. "What we found was that some of these tRNA molecules are much more efficient at being loaded with amino acids, while others are less so," Subramaniam said. "If these tRNA molecules can't deliver the amino acid to where it needs to be, the cell cannot manufacture the proteins it needs. In an environment where amino acids are in short supply, that ability to hold onto them becomes very important." While the system helps cells to make certain proteins efficiently under stressful conditions, it also acts as a biological failsafe, allowing the near-complete shutdown in the production of other proteins as a way to preserve limited resources.

Read more at: http://phys.org/news/2013-01-hidden-genetic-code-key-differences.html#jCp

Genome complexity; 4 stranded DNA

by David Turell @, Tuesday, January 22, 2013, 21:00 (2072 days ago) @ David Turell

Genome complexity; lncRNA

by David Turell @, Friday, January 25, 2013, 14:41 (2069 days ago) @ David Turell

Learn about long non-coding RNA. Found in junk DNA they are important in embryology. Thre are so many layers of coding in the genome, but it all happened by chance?

http://medicalxpress.com/news/2013-01-non-coding-rna-molecules-differentiation-embryoni...

Genome complexity; Transcription factors

by David Turell @, Monday, January 28, 2013, 15:57 (2066 days ago) @ David Turell

The reason we have so few genes is the multiplicity of transcription factors so genes can do many jobs at once. The higher the animal on the evolution bush, the more factors:

http://www.sciencedaily.com/releases/2013/01/130117133356.htm

Genome complexity; Embryology

by David Turell @, Tuesday, January 29, 2013, 15:37 (2065 days ago) @ David Turell

Long non-coding RNA helps build organs. Here the heart is described:

http://phys.org/news/2013-01-epigenetic-cardiogenesis-non-coding-rna-essential.html

Genome complexity; gene expression

by David Turell @, Monday, February 04, 2013, 15:54 (2059 days ago) @ David Turell

Gene control is so complex we cannot imitate it in the lab, but we can do simple things:

http://www.sciencedaily.com/releases/2013/02/130203145558.htm

Genome complexity; epigenetic gene expression

by David Turell @, Monday, February 04, 2013, 18:26 (2059 days ago) @ David Turell

You tube presentation of epigenetic markkers changing expression:

http://www.youtube.com/watch?feature=player_detailpage&v=nygyUMODV7Y

Genome complexity; garbage removal

by David Turell @, Thursday, February 07, 2013, 14:48 (2056 days ago) @ David Turell

Cells make proteins that must be destroyed; cells also make RNA's that guide processes and then must be destroyed or the cell will become so stuffed it won't function. There is a proteosome for proteins and an exosome for RNAs:

"The structure of this complex allowed the scientists to understand how the exosome works. "It is quite an elaborate machine: the exosome complex forms a hollow barrel formed by nine different proteins through which RNA molecules are threaded to reach a tenth protein, the catalytic subunit that then shreds the RNA into pieces," says Debora Makino. The barrel is essential for this process because it helps to unwind the RNA and prepares it for shredding. "Cells lacking any of the ten proteins do not survive and this shows that not only the catalytic subunit but also the entire barrel is critical for the function of the exosome," Makino explains." (my bold)

http://www.sciencedaily.com/releases/2013/02/130204094606.htm

This fits Behe's definition of 'irreducable complexity', a structure that cannot have evolved one protein step at a time.

Further these processes are found in Archaea and other bacteria, again showing how complex the original living cells had to be.

Genome complexity; chromosome protection

by David Turell @, Thursday, February 07, 2013, 15:24 (2056 days ago) @ David Turell

:TRF2 is a complex protein with four functional domains (regions). Okamoto probed the specific functions of these four domains by creating artificial TRF2-like proteins—in which one or more functional domains were replaced with non-functional "dummy" domains. By studying how these artificial TRF2s functioned in cells, he could determine the separate functions of each individual domain."

Read more at: http://medicalxpress.com/news/2013-02-chromosomes-loose.html#jCp

Not a very simple protein. It keeps chromosomes separated.

Genome complexity; new study techniques

by David Turell @, Friday, February 08, 2013, 15:46 (2055 days ago) @ David Turell

From electron microscopy with dyes and fluoressing molecules to holography!

http://www.sciencedaily.com/releases/2013/02/130207172205.htm

Genome complexity; epigenetics

by David Turell @, Tuesday, February 12, 2013, 21:09 (2051 days ago) @ David Turell

A You tube video of the complexity involved in epigenetic adaptational controls which can lead to inheritable changes. This removes a major tenet of Darwinism that evolution is entirely at random and a chance mechanism that never implies purpose. Organisms can adapt and it may be purposeful most of the time. However, chance mutations do occur and must have some effect although most chance mutationsd have been found to be deleterious:

http://www.youtube.com/watch?feature=player_detailpage&v=52d5jWK1vdc

Science progress seems to be on God's side.

Genome complexity; epigenetics

by dhw, Thursday, February 14, 2013, 15:09 (2049 days ago) @ David Turell

DAVID: A You tube video of the complexity involved in epigenetic adaptational controls which can lead to inheritable changes. This removes a major tenet of Darwinism that evolution is entirely at random and a chance mechanism that never implies purpose. Organisms can adapt and it may be purposeful most of the time. However, chance mutations do occur and must have some effect although most chance mutations have been found to be deleterious:

http://www.youtube.com/watch?feature=player_detailpage&v=52d5jWK1vdc

Science progress seems to be on God's side.

If the speaker's monotone doesn't send you to sleep, this is stirring stuff! He seems to lay emphasis, though, on environmental stress as a major factor, and in your very helpful summary, David, you also emphasize adaptation. What interests me far more is innovation, and although we have no idea to what extent the two overlap, it seems to me that adaptation is more likely to preserve existing species, whereas innovation obviously leads to new ones. (By species, I don't mean varieties of, say, finch, but different organisms like elephants, eagles, ants, sharks, humans.) The speaker does mention macroevolution, but still talks of it being induced by the environment, which again suggests adaptation. That is why, in my amateur way, I keep pushing the idea that the mechanism for change ... whether adaptation or innovation ... has a built-in inventiveness which enables organisms not only to respond to stress for the sake of survival, but also to invent new organs that will take advantage of new environments. Without innovation, there can be no evolution!

You and I have agreed, David, that random mutations and gradualism are major weaknesses in Darwin's theory, and so I like the speaker's conclusion ... that we now need a theory that will combine Darwinian, Lamarckian and saltational processes. He also mentioned the vitally important element of "cooperation" (so he could have added Margulisian to his list). Well, how about "the intelligent genome"? It fits in with all that we know about evolution, and it appears to fit in with all the latest discoveries concerning genetics and epigenetics. You will quite rightly ask where the intelligence comes from (you always do!), but the focus here is on how evolution works, and that for me is an end in itself.

Genome complexity; epigenetics: Lamarck is back

by David Turell @, Wednesday, June 01, 2016, 01:34 (846 days ago) @ dhw

This essay makes some interesting remarks about Lamarck and epigenetics, and the problems Darwin adherents and atheists are having:

http://www.abc.net.au/radionational/programs/ockhamsrazor/descartes-to-dawkins-history-...

"One important person to describe living things self-transforming machines was 18th century French naturalist, Jean-Baptiste Lamarck.

"You might have heard of Lamarck as a crackpot: the man who said that giraffes' long necks are due to reaching high-up fruit. You may also have heard that Darwin got rid of Lamarck's idea of the inheritance of acquired characteristics. But in fact that's not true at all. Darwin was very much influenced by Lamarck.

"In particular, Charles Darwin believed in the inheritance of acquired characteristics, or what he generally called the effects of use and disuse—for example, that moles eventually evolved to be blind on account of not using their eyes.

"In that sense, Darwin was very much a Lamarckian. So why did we all learn in high school biology class that Lamarck was crazy and Darwin got rid of all his crazy ideas?

"Lamarck's description of evolution as resulting from living organisms' own agency threatened God's monopoly on creation. In the wake of the French Revolution, this made Lamarck seemed like a very dangerous sort of Frenchman.

"Around the turn of the 20th century, Darwinists wanting to promote a strong and viable Darwinism started trying to eradicate every trace of Lamarckism.

***

"Weismann cut the tails off mice in order to show that their offspring had perfectly normal tails. He presented his findings as a definitive refutation of Lamarck. His mice continue to appear in biology textbooks as just that.

"But of course, they had no bearing on Lamarck's theory at all—since Lamarck believed, as I've said, that organisms transformed themselves by acts of will, by habits and behaviours.

"You could hardly call having your tail lopped off an act of will, a habit or a behaviour.

***

"Today's neo-Darwinists—people such as Richard Dawkins and Daniel Dennett—are really Weismannians (in fact, Dawkins has called himself an ‘extreme Weismannian').

"Even outside of evolutionary biology, some of the most influential thinkers and writers in biology and cognitive science today have adopted the Weismannian view that living organisms are essentially passive, made of dumb and inert mechanical parts.

"Cognitive scientist Steven Pinker is an example: he has written that the human mind can be reduced to ‘armies of idiots'—mindless sub-routines in the brain that merely do what they are programmed to.

"The idea that mind can be reduced to mindlessness and living agency to passive mechanical parts is a central tenet of the New Atheism movement.

***

"The engineering or design model of living nature, which they have all adopted, implies a designer. If you truly want to eliminate the designer, you need to naturalise his agency: allow the possibility that living nature has the agency to create and transform itself. (my bold)

***

"What's especially fascinating to me is that Lamarckism has been making a comeback in the last 10 or 15 years: biologists have been finding various ways in which changes in an individual organism can be inherited.

"The field of epigenetics is largely devoted to this. Epigenetics studies all the ways in which factors outside the DNA shape the way an organism is formed, and many of these epigenetic factors can change in heritable ways.

"In this sense, an organism might have agency with regard to its evolutionary destiny, just as Lamarck thought."

Comment: Note my bold. This is the crux of my discussion with dhw. We still don't know exactly how the epigenetic adaptations we see can lead to new species, if at all.

Genome complexity; epigenetics: Lamarck is back

by dhw, Wednesday, June 01, 2016, 13:22 (846 days ago) @ David Turell

DAVID: This essay makes some interesting remarks about Lamarck and epigenetics, and the problems Darwin adherents and atheists are having:

http://www.abc.net.au/radionational/programs/ockhamsrazor/descartes-to-dawkins-history-...

Thank you for this revealing contribution to our debate. The quotes below make it very clear that so-called Darwin adherents have deliberately twisted Darwin's beliefs to fit in with their own. Shame on them.

QUOTES: "You might have heard of Lamarck as a crackpot: the man who said that giraffes' long necks are due to reaching high-up fruit. You may also have heard that Darwin got rid of Lamarck's idea of the inheritance of acquired characteristics. But in fact that's not true at all. Darwin was very much influenced by Lamarck.
"In particular, Charles Darwin believed in the inheritance of acquired characteristics, or what he generally called the effects of use and disuse—for example, that moles eventually evolved to be blind on account of not using their eyes.
"In that sense, Darwin was very much a Lamarckian. So why did we all learn in high school biology class that Lamarck was crazy and Darwin got rid of all his crazy ideas?
"Lamarck's description of evolution as resulting from living organisms' own agency threatened God's monopoly on creation.”

Please note “own agency” - the active role organisms may play in their own evolution. The next quote provides a problem for your own theory:

QUOTE: "Even outside of evolutionary biology, some of the most influential thinkers and writers in biology and cognitive science today have adopted the Weismannian view that living organisms are essentially passive, made of dumb and inert mechanical parts.”

This is also your own theistic view when you revert to your theory of divine preprogramming. According to that, all the “parts” can do is passively obey the instructions laid down for them by your God 3.8 billion years ago, or let themselves be dabbled with.

QUOTE: "The engineering or design model of living nature, which they have all adopted, implies a designer. If you truly want to eliminate the designer, you need to naturalise his agency: allow the possibility that living nature has the agency to create and transform itself." (David's bold)
David's comment: Note my bold. This is the crux of my discussion with dhw. We still don't know exactly how the epigenetic adaptations we see can lead to new species, if at all.

Your bold is certainly true: if you want to eliminate the designer, you have to eliminate the designer. But allowing the possibility that organisms have the “agency” to transform themselves does not by any means eliminate the designer, since this still leaves wide open the question of how life began, and how organisms came to possess the “agency” to transform themselves. Your bold is not the crux of our discussion, because my hypothesis that evolution develops through the “agency” of the organisms themselves is NOT a means of eliminating the designer. It explains the higgledy-piggledy bush, and is an alternative to your hypothesis that your God preprogrammed or dabbled every innovation (and natural wonder) in the course of life's history for the purpose of “balancing nature” in order to produce and feed humans.

Genome complexity; epigenetics: Lamarck is back

by David Turell @, Wednesday, June 01, 2016, 22:48 (846 days ago) @ dhw

dhw: "Lamarck's description of evolution as resulting from living organisms' own agency threatened God's monopoly on creation.”[/i]

Please note “own agency” - the active role organisms may play in their own evolution. The next quote provides a problem for your own theory:

QUOTE: "Even outside of evolutionary biology, some of the most influential thinkers and writers in biology and cognitive science today have adopted the Weismannian view that living organisms are essentially passive, made of dumb and inert mechanical parts.”

This is also your own theistic view when you revert to your theory of divine preprogramming. According to that, all the “parts” can do is passively obey the instructions laid down for them by your God 3.8 billion years ago, or let themselves be dabbled with.

That is not a problem for me, but it is for you. My problem with that assumption is I can't discern how God controls evolution whether by pre-programming, or dabbling or both, but I'm content that He is in control.


QUOTE: "The engineering or design model of living nature, which they have all adopted, implies a designer. If you truly want to eliminate the designer, you need to naturalise his agency: allow the possibility that living nature has the agency to create and transform itself." (David's bold)
David's comment: Note my bold. This is the crux of my discussion with dhw. We still don't know exactly how the epigenetic adaptations we see can lead to new species, if at all.

dhw: Your bold is certainly true: if you want to eliminate the designer, you have to eliminate the designer. But allowing the possibility that organisms have the “agency” to transform themselves does not by any means eliminate the designer, since this still leaves wide open the question of how life began, and how organisms came to possess the “agency” to transform themselves. Your bold is not the crux of our discussion, because my hypothesis that evolution develops through the “agency” of the organisms themselves is NOT a means of eliminating the designer. It explains the higgledy-piggledy bush, and is an alternative to your hypothesis that your God preprogrammed or dabbled every innovation (and natural wonder) in the course of life's history for the purpose of “balancing nature” in order to produce and feed humans.

Of course, your analysis is excellent, IF organisms can develop the evolutionary agency on their own. In my view they can't as in the essay. But my complexification theory explains the bush also, because it is a variation on your theme.

Genome complexity; epigenetics: Lamarck is back

by dhw, Thursday, June 02, 2016, 12:49 (845 days ago) @ David Turell

QUOTE: "Even outside of evolutionary biology, some of the most influential thinkers and writers in biology and cognitive science today have adopted the Weismannian view that living organisms are essentially passive, made of dumb and inert mechanical parts.”
Dhw: This is also your own theistic view when you revert to your theory of divine preprogramming. According to that, all the “parts” can do is passively obey the instructions laid down for them by your God 3.8 billion years ago, or let themselves be dabbled with.

DAVID: That is not a problem for me, but it is for you. My problem with that assumption is I can't discern how God controls evolution whether by pre-programming, or dabbling or both, but I'm content that He is in control.

Once again you are turning your back on the “free mechanism” you had accepted on Monday 30 May. However, all this highlights a basic contradiction in the essay you quoted: the author stated that Lamarck was dangerous in his time because his “description of evolution as resulting from living organism's own agency threatened God's monopoly on creation.” And yet he goes on to say that Darwinists and now neo-Darwinists (atheists) like Dawkins have tried to eradicate Lamarckism! As I see it, Lamarckism would actually help the atheist cause by adding purposeful change to random mutations, and so I can only assume that the opposition is purely scientific (lack of evidence) rather than agenda-driven. But since you say the subject creates problems for atheists, perhaps you can tell us their other objections. On the other hand, Lamarckism does not exclude the existence of God as the maker of the inventive mechanism, but it does create a challenge to your preprogramming theory. Epigenetics seems to be the new form of Lamarckism, and even you admit you don't know how far the process might extend - but that doesn't matter to you, because you are content that God either preprogrammed or dabbled every single innovation.

dhw: Your bold is not the crux of our discussion, because my hypothesis that evolution develops through the “agency” of the organisms themselves is NOT a means of eliminating the designer. It explains the higgledy-piggledy bush, and is an alternative to your hypothesis […].
DAVID: Of course, your analysis is excellent, IF organisms can develop the evolutionary agency on their own. In my view they can't as in the essay. But my complexification theory explains the bush also, because it is a variation on your theme.

Your swift reversion to your God programming every complexity is not a variation on my theme at all. It is the exact opposite. All you are now saying is that the bush is higgledy-piggledy because God deliberately preprogrammed or dabbled every twig (just for the sake of complexity). I am saying it is higgledy-piggledy because (theistic version) God gave organisms the freedom to create their own complexities.

Genome complexity; epigenetics: Lamarck is back

by David Turell @, Friday, June 03, 2016, 02:03 (844 days ago) @ dhw

QUOTE: "Even outside of evolutionary biology, some of the most influential thinkers and writers in biology and cognitive science today have adopted the Weismannian view that living organisms are essentially passive, made of dumb and inert mechanical parts.”
Dhw: This is also your own theistic view when you revert to your theory of divine preprogramming. According to that, all the “parts” can do is passively obey the instructions laid down for them by your God 3.8 billion years ago, or let themselves be dabbled with.

DAVID: That is not a problem for me, but it is for you. My problem with that assumption is I can't discern how God controls evolution whether by pre-programming, or dabbling or both, but I'm content that He is in control.

dhw: Once again you are turning your back on the “free mechanism” you had accepted on Monday 30 May.... Epigenetics seems to be the new form of Lamarckism, and even you admit you don't know how far the process might extend - but that doesn't matter to you, because you are content that God either preprogrammed or dabbled every single innovation.

My mind is still mulling. I'm back on the complexity track today, as you will see.


dhw: Your swift reversion to your God programming every complexity is not a variation on my theme at all. It is the exact opposite. All you are now saying is that the bush is higgledy-piggledy because God deliberately preprogrammed or dabbled every twig (just for the sake of complexity). I am saying it is higgledy-piggledy because (theistic version) God gave organisms the freedom to create their own complexities.

I'm agreeing with you. I like the idea of complexity for complexity's sake, with God's dabbling after the complexity appears, as He sees necessary.

Genome complexity; epigenetics: Lamarck is back

by David Turell @, Thursday, August 17, 2017, 15:32 (404 days ago) @ David Turell

Another essay on how important epigenetics is:

https://aeon.co/essays/on-epigenetics-we-need-both-darwin-s-and-lamarck-s-theories?utm_...

"One of the most common such processes is ‘DNA methylation’, in which molecular components called methyl groups (made of methane) attach to DNA, turning genes on or off, and regulating the level of gene expression. Environmental factors such as temperature or emotional stress have been shown to alter DNA methylation, and these changes can be permanently programmed and inherited over generations – a process known as epigenetic transgenerational inheritance.

"Another major epigenetic process discovered in recent years is ‘histone modification’.
Histones are proteins that attach to and alter the structure of DNA, which in turn wraps around the histones like beads on a string. The combination of DNA and histone together has been called ‘chromatin structures’ – and the coils, loops and twists in chromatin structures in response to environmental stress can permanently alter gene expression as well.

"More recently, researchers have documented ‘RNA methylation’ in which methyl groups attach to the genetic helper molecules, in the process altering gene expression and subsequent protein production for generations down the line. Likewise, the action of so-called ‘non-coding RNA’, small RNA molecules that bind to DNA, RNA and proteins, also alter the expression of genes, independent of DNA sequence.

"All of these epigenetic mechanisms are critical and have unique roles in the molecular regulation of how DNA functions. The regulation of biology, it follows, will never involve a ‘genetic-only process’, nor an ‘epigenetic-only process’. Instead, the processes of epigenetics and genetics are completely integrated. One does not work without the other.

***

"In another recent study, we examined evolution on the macro-evolutionary scale – speciation. One of the classic examples of speciation involves Darwin’s finches in the Galapagos Islands. A group of finches radiated out from a single species to become 16 different species of varying size and with different traits such as altered beak structure. Our team and collaborators set out to examine the DNA from five of those distinct species. We observed DNA sequence mutations from one species to the next, but the epigenetic changes in DNA methylation (epimutations) were higher in number and more correlated with the phylogenetic (family tree) distance between the species. Although the field of evolution is currently focused on neo-Darwinian genetic concepts, our findings suggest that epigenetics also has a role in the speciation and evolution of Darwin’s finches.

***

"Nearly all types of genetic mutations are known to have a precursor epigenetic change that increases the susceptibility to develop that mutation. We observed that direct environmental exposure in the first generation had epigenetic changes and no genetic mutations but, transgenerationally, an increase in genetic mutations was identified. Since environmental epigenetics can promote both trait variation and mutations, it accelerates the engine of evolution in a way that Darwinian mechanisms alone cannot.

***

"I’m convinced that we have reached the point where a paradigm shift is due. Accepting that epigenetics plays a role in evolution does not topple the science of genetics; embracing neo-Lamarckian ideas does nothing to challenge classic neo-Darwinian theory. The accepted sciences are essential and accurate, but part of a bigger, more nuanced story that expands our understanding and integrates all our observations into a cohesive whole. The unified theory explains how the environment can both act to directly influence phenotypic variation and directly facilitate natural selection,

***

"A unified theory of evolution should combine both neo-Lamarckian and neo-Darwinian aspects to expand our understanding of how environment impacts evolution. The contributions of Lamarck more than 200 years ago should not be discounted because of Darwin, but instead integrated to generate a more impactful and insightful theory. Likewise, genetics and epigenetics must not be seen as conflicting areas, but instead, integrated to provide a broader repertoire of molecular factors to explain how life is controlled."

Comment: Lamarck lives. The author is an active research scientist in the field of epigenetics.

Genome complexity; epigenetics: Lamarck is back

by dhw, Friday, August 18, 2017, 13:36 (403 days ago) @ David Turell

DAVID: Another essay on how important epigenetics is:

https://aeon.co/essays/on-epigenetics-we-need-both-darwin-s-and-lamarck-s-theories?utm_...

QUOTE: In another recent study, we examined evolution on the macro-evolutionary scale – speciation. One of the classic examples of speciation involves Darwin’s finches in the Galapagos Islands.

I am a convinced evolutionist, but I find this kind of vocabulary irritating because it glosses over the problem of the very word “speciation”. Darwin’s finches were variations, and the explanation for those variations is wonderfully logical. But it offers no explanation for the innovations necessary to make single cells develop into elephants, eagles, sharks and humans.

QUOTE: A unified theory of evolution should combine both neo-Lamarckian and neo-Darwinian aspects to expand our understanding of how environment impacts evolution.

I agree 100%, and the major question is what is the mechanism that enables organisms to respond to the environment not just by adaptation but also by innovation.

Genome complexity; epigenetics: Lamarck is back

by David Turell @, Friday, August 18, 2017, 15:38 (403 days ago) @ dhw

DAVID: Another essay on how important epigenetics is:

https://aeon.co/essays/on-epigenetics-we-need-both-darwin-s-and-lamarck-s-theories?utm_...

QUOTE: In another recent study, we examined evolution on the macro-evolutionary scale – speciation. One of the classic examples of speciation involves Darwin’s finches in the Galapagos Islands.

dhw: I am a convinced evolutionist, but I find this kind of vocabulary irritating because it glosses over the problem of the very word “speciation”. Darwin’s finches were variations, and the explanation for those variations is wonderfully logical. But it offers no explanation for the innovations necessary to make single cells develop into elephants, eagles, sharks and humans.

QUOTE: A unified theory of evolution should combine both neo-Lamarckian and neo-Darwinian aspects to expand our understanding of how environment impacts evolution.

dhw: I agree 100%, and the major question is what is the mechanism that enables organisms to respond to the environment not just by adaptation but also by innovation.

Yes, speciation is not explained. Epigenetics does not explain the big gaps in the fossil record.

Genome complexity; epigenetics: Lamarck is back

by David Turell @, Wednesday, August 29, 2018, 20:04 (27 days ago) @ David Turell

Peter Ward in a new book:

http://nautil.us/issue/63/horizons/why-the-earth-has-fewer-species-than-we-think

"More and more, biologists are discovering that organisms thought to be different species are, in fact, but one. A recent example is that the formerly accepted two species of giant North American mammoths (the Columbian mammoth and the woolly mammoth) were genetically the same but the two had phenotypes determined by environment.

"Epigenetics (or heritable epigenetics, or neo-Lamarckism) is a series of different processes that can cause evolutionary changes as well as dictate how organisms develop from a single fertilized egg (in the case of sexually reproducing organisms, at least) to what we look like as adults. Some say it’s just a minor tweak of already understood processes and that it’s of little importance in the broader scheme of evolutionary change or the past or even future history of life. But to others epigenetics, while still poorly understood, is potentially of far greater importance than mainstream evolutionary theory, and mainstream evolutionists have heretofore accepted that. To a few, its ongoing discovery is causing an unfolding scientific revolution. But the discoveries have not happened evenly among the many fields within what we call “biology.” The great breakthroughs have mainly been studies looking at cells, and the molecules within cells, including DNA and RNA and other aspects of genetics. But to date there has been little if any progress in tying epigenetic change to the many events evidenced by fossils and the fossil record."

Here’s where epigenetics differs from traditional Darwinian evolution:

"The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”

Comment: This fits Tony's idea about species.

Genome complexity; epigenetics: Lamarck is back

by Balance_Maintained @, U.S.A., Wednesday, August 29, 2018, 22:22 (27 days ago) @ David Turell

Peter Ward in a new book:

http://nautil.us/issue/63/horizons/why-the-earth-has-fewer-species-than-we-think

"More and more, biologists are discovering that organisms thought to be different species are, in fact, but one. A recent example is that the formerly accepted two species of giant North American mammoths (the Columbian mammoth and the woolly mammoth) were genetically the same but the two had phenotypes determined by environment.

"Epigenetics (or heritable epigenetics, or neo-Lamarckism) is a series of different processes that can cause evolutionary changes as well as dictate how organisms develop from a single fertilized egg (in the case of sexually reproducing organisms, at least) to what we look like as adults. Some say it’s just a minor tweak of already understood processes and that it’s of little importance in the broader scheme of evolutionary change or the past or even future history of life. But to others epigenetics, while still poorly understood, is potentially of far greater importance than mainstream evolutionary theory, and mainstream evolutionists have heretofore accepted that. To a few, its ongoing discovery is causing an unfolding scientific revolution. But the discoveries have not happened evenly among the many fields within what we call “biology.” The great breakthroughs have mainly been studies looking at cells, and the molecules within cells, including DNA and RNA and other aspects of genetics. But to date there has been little if any progress in tying epigenetic change to the many events evidenced by fossils and the fossil record."

Here’s where epigenetics differs from traditional Darwinian evolution:

"The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”

Comment: This fits Tony's idea about species.

It would explain point eggs...

--
Without darkness there can be no light, no truth without lies.

Genome complexity; epigenetics: Lamarck is back

by David Turell @, Thursday, August 30, 2018, 00:58 (26 days ago) @ Balance_Maintained

Peter Ward in a new book:

http://nautil.us/issue/63/horizons/why-the-earth-has-fewer-species-than-we-think

"More and more, biologists are discovering that organisms thought to be different species are, in fact, but one. A recent example is that the formerly accepted two species of giant North American mammoths (the Columbian mammoth and the woolly mammoth) were genetically the same but the two had phenotypes determined by environment.

"Epigenetics (or heritable epigenetics, or neo-Lamarckism) is a series of different processes that can cause evolutionary changes as well as dictate how organisms develop from a single fertilized egg (in the case of sexually reproducing organisms, at least) to what we look like as adults. Some say it’s just a minor tweak of already understood processes and that it’s of little importance in the broader scheme of evolutionary change or the past or even future history of life. But to others epigenetics, while still poorly understood, is potentially of far greater importance than mainstream evolutionary theory, and mainstream evolutionists have heretofore accepted that. To a few, its ongoing discovery is causing an unfolding scientific revolution. But the discoveries have not happened evenly among the many fields within what we call “biology.” The great breakthroughs have mainly been studies looking at cells, and the molecules within cells, including DNA and RNA and other aspects of genetics. But to date there has been little if any progress in tying epigenetic change to the many events evidenced by fossils and the fossil record."

Here’s where epigenetics differs from traditional Darwinian evolution:

"The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”

DAvid: Comment: This fits Tony's idea about species.


Tony: It would explain point eggs...

If only an epigenetic change in DNA can do it.

Genome complexity; epigenetics: Lamarck is back

by dhw, Thursday, August 30, 2018, 08:12 (26 days ago) @ David Turell

QUOTE: The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”

DAVID: This fits Tony's idea about species.

It fits the idea that environmental change is the trigger for organismal change, whether adaptation or innovation. I see no hint of advance planning here, or of new organisms suddenly appearing out of nowhere.

Genome complexity; epigenetics: Lamarck is back

by David Turell @, Thursday, August 30, 2018, 18:02 (26 days ago) @ dhw

QUOTE: The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”

DAVID: This fits Tony's idea about species.

dhw: It fits the idea that environmental change is the trigger for organismal change, whether adaptation or innovation. I see no hint of advance planning here, or of new organisms suddenly appearing out of nowhere.

Advanced planning has evidence in a huge gap like the Cambrian Explosion. No explanation as yet for the Cambrian animals who appear out of nowhere

Genome complexity; epigenetics: Lamarck is back

by dhw, Friday, August 31, 2018, 13:42 (25 days ago) @ David Turell

QUOTE: The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”

DAVID: This fits Tony's idea about species.

dhw: It fits the idea that environmental change is the trigger for organismal change, whether adaptation or innovation. I see no hint of advance planning here, or of new organisms suddenly appearing out of nowhere.

DAVID: Advanced planning has evidence in a huge gap like the Cambrian Explosion. No explanation as yet for the Cambrian animals who appear out of nowhere.

You claimed that Lamarckian change, as quoted above, fitted Tony’s ideas about species. These include advance planning and new organisms appearing out of nowhere. I have simply pointed out that Lamarckian change, as quoted above, makes no mention of advance planning or of new organisms coming out of nowhere. So how does it fit Tony's ideas about species?

Genome complexity; epigenetics: Lamarck is back

by David Turell @, Friday, August 31, 2018, 19:18 (25 days ago) @ dhw

QUOTE: The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”

DAVID: This fits Tony's idea about species.

dhw: It fits the idea that environmental change is the trigger for organismal change, whether adaptation or innovation. I see no hint of advance planning here, or of new organisms suddenly appearing out of nowhere.

DAVID: Advanced planning has evidence in a huge gap like the Cambrian Explosion. No explanation as yet for the Cambrian animals who appear out of nowhere.

dhw: You claimed that Lamarckian change, as quoted above, fitted Tony’s ideas about species. These include advance planning and new organisms appearing out of nowhere. I have simply pointed out that Lamarckian change, as quoted above, makes no mention of advance planning or of new organisms coming out of nowhere. So how does it fit Tony's ideas about species?

Ward's point is some species are really Lamarckian adaptations of existing species and therefore not a new species. Tony's 'staged advances' from existing forms is simply a similar thought pattern I think. The evidence for advanced planning lies in the Cambrian gap in phenotypes.

Genome complexity; epigenetics: Lamarck is back

by Balance_Maintained @, U.S.A., Friday, August 31, 2018, 21:14 (25 days ago) @ David Turell

QUOTE: The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”

DAVID: This fits Tony's idea about species.

dhw: It fits the idea that environmental change is the trigger for organismal change, whether adaptation or innovation. I see no hint of advance planning here, or of new organisms suddenly appearing out of nowhere.

DAVID: Advanced planning has evidence in a huge gap like the Cambrian Explosion. No explanation as yet for the Cambrian animals who appear out of nowhere.

dhw: You claimed that Lamarckian change, as quoted above, fitted Tony’s ideas about species. These include advance planning and new organisms appearing out of nowhere. I have simply pointed out that Lamarckian change, as quoted above, makes no mention of advance planning or of new organisms coming out of nowhere. So how does it fit Tony's ideas about species?


David: Ward's point is some species are really Lamarckian adaptations of existing species and therefore not a new species. Tony's 'staged advances' from existing forms is simply a similar thought pattern I think. The evidence for advanced planning lies in the Cambrian gap in phenotypes.

Actually, it was more to the point that we are finding fewer 'kinds' and are still able to account for the programmatic variation in a mechanical way. Further, the interplay between genetic stability and epigenetic changes causing the bushy 'leaves' that hid the fact that there are only a few branches is far too complex to not have been designed.

DNA is incredibly complex and informationally dense. Epigenetics will likely prove to be incredibly complex and informationally dense as we understand it more. To have such incredible finesse and control, complete with safeguards and redundancies and repair systems is absolutely not possible by chance.

In the end, we will find periodic creation of flora and fauna in limited branches at the cusp of great atmospheric or geologic changes in which the arriving types play a significant roll in the further development of the earth, such as balancing CO2 and O2 and other gasses in the atmosphere, or perhaps bacteria creating oil resevoirs as a form of planetary lubricant to deal with the internal stresses caused by the start of plate tectonics.

I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.

--
Without darkness there can be no light, no truth without lies.

Genome complexity; epigenetics: Lamarck is back

by David Turell @, Friday, August 31, 2018, 23:54 (25 days ago) @ Balance_Maintained

dhw: You claimed that Lamarckian change, as quoted above, fitted Tony’s ideas about species. These include advance planning and new organisms appearing out of nowhere. I have simply pointed out that Lamarckian change, as quoted above, makes no mention of advance planning or of new organisms coming out of nowhere. So how does it fit Tony's ideas about species?

David: Ward's point is some species are really Lamarckian adaptations of existing species and therefore not a new species. Tony's 'staged advances' from existing forms is simply a similar thought pattern I think. The evidence for advanced planning lies in the Cambrian gap in phenotypes.


Tony: Actually, it was more to the point that we are finding fewer 'kinds' and are still able to account for the programmatic variation in a mechanical way. Further, the interplay between genetic stability and epigenetic changes causing the bushy 'leaves' that hid the fact that there are only a few branches is far too complex to not have been designed.

DNA is incredibly complex and informationally dense. Epigenetics will likely prove to be incredibly complex and informationally dense as we understand it more. To have such incredible finesse and control, complete with safeguards and redundancies and repair systems is absolutely not possible by chance.

In the end, we will find periodic creation of flora and fauna in limited branches at the cusp of great atmospheric or geologic changes in which the arriving types play a significant roll in the further development of the earth, such as balancing CO2 and O2 and other gasses in the atmosphere, or perhaps bacteria creating oil resevoirs as a form of planetary lubricant to deal with the internal stresses caused by the start of plate tectonics.

I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.

I agree with you. The balance between every individual in studies of eco-niches shows that top predators are a requirement, i.e., the wolves of Yellowstone. Everyone at every level has a role to play.

Genome complexity; epigenetics: Lamarck is back

by dhw, Saturday, September 01, 2018, 10:00 (24 days ago) @ David Turell

dhw: You claimed that Lamarckian change, as quoted above, fitted Tony’s ideas about species. These include advance planning and new organisms appearing out of nowhere. I have simply pointed out that Lamarckian change, as quoted above, makes no mention of advance planning or of new organisms coming out of nowhere. So how does it fit Tony's ideas about species?

DAVID: Ward's point is some species are really Lamarckian adaptations of existing species and therefore not a new species. Tony's 'staged advances' from existing forms is simply a similar thought pattern I think.

That concerns the definition of species, which I think we have all agreed on now as referring to organisms which cannot interbreed. I thought you were referring to Tony’s ideas about species being planned and appearing out of nowhere, so I’m glad we’ve clarified the misunderstanding.

TONY: DNA is incredibly complex and informationally dense. Epigenetics will likely prove to be incredibly complex and informationally dense as we understand it more. To have such incredible finesse and control, complete with safeguards and redundancies and repair systems is absolutely not possible by chance.

Until we get a supporter of the chance theory to join us, there will be no discussion on this. The only open question is how design comes about.

TONY: In the end, we will find periodic creation of flora and fauna in limited branches at the cusp of great atmospheric or geologic changes in which the arriving types play a significant roll in the further development of the earth, such as balancing CO2 and O2 and other gasses in the atmosphere, or perhaps bacteria creating oil resevoirs as a form of planetary lubricant to deal with the internal stresses caused by the start of plate tectonics.
I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.

And how do you propose to test the fundamental function performed by the millions of life forms (root types and their variants) that have disappeared?

Genome complexity; epigenetics: Lamarck is back

by David Turell @, Saturday, September 01, 2018, 15:25 (24 days ago) @ dhw

dhw: You claimed that Lamarckian change, as quoted above, fitted Tony’s ideas about species. These include advance planning and new organisms appearing out of nowhere. I have simply pointed out that Lamarckian change, as quoted above, makes no mention of advance planning or of new organisms coming out of nowhere. So how does it fit Tony's ideas about species?

DAVID: Ward's point is some species are really Lamarckian adaptations of existing species and therefore not a new species. Tony's 'staged advances' from existing forms is simply a similar thought pattern I think.

dhw:v That concerns the definition of species, which I think we have all agreed on now as referring to organisms which cannot interbreed. I thought you were referring to Tony’s ideas about species being planned and appearing out of nowhere, so I’m glad we’ve clarified the misunderstanding.

TONY: DNA is incredibly complex and informationally dense. Epigenetics will likely prove to be incredibly complex and informationally dense as we understand it more. To have such incredible finesse and control, complete with safeguards and redundancies and repair systems is absolutely not possible by chance.

dhw: Until we get a supporter of the chance theory to join us, there will be no discussion on this. The only open question is how design comes about.

TONY: In the end, we will find periodic creation of flora and fauna in limited branches at the cusp of great atmospheric or geologic changes in which the arriving types play a significant roll in the further development of the earth, such as balancing CO2 and O2 and other gasses in the atmosphere, or perhaps bacteria creating oil resevoirs as a form of planetary lubricant to deal with the internal stresses caused by the start of plate tectonics.

I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.[/i]


dhw: And how do you propose to test the fundamental function performed by the millions of life forms (root types and their variants) that have disappeared?

Evolution implies replacement and in the case of evolution from simple to more complex

Genome complexity; epigenetics: Lamarck is back

by Balance_Maintained @, U.S.A., Saturday, September 01, 2018, 23:03 (24 days ago) @ David Turell

dhw: You claimed that Lamarckian change, as quoted above, fitted Tony’s ideas about species. These include advance planning and new organisms appearing out of nowhere. I have simply pointed out that Lamarckian change, as quoted above, makes no mention of advance planning or of new organisms coming out of nowhere. So how does it fit Tony's ideas about species?

DAVID: Ward's point is some species are really Lamarckian adaptations of existing species and therefore not a new species. Tony's 'staged advances' from existing forms is simply a similar thought pattern I think.

dhw:v That concerns the definition of species, which I think we have all agreed on now as referring to organisms which cannot interbreed. I thought you were referring to Tony’s ideas about species being planned and appearing out of nowhere, so I’m glad we’ve clarified the misunderstanding.

TONY: DNA is incredibly complex and informationally dense. Epigenetics will likely prove to be incredibly complex and informationally dense as we understand it more. To have such incredible finesse and control, complete with safeguards and redundancies and repair systems is absolutely not possible by chance.

dhw: Until we get a supporter of the chance theory to join us, there will be no discussion on this. The only open question is how design comes about.

TONY: In the end, we will find periodic creation of flora and fauna in limited branches at the cusp of great atmospheric or geologic changes in which the arriving types play a significant roll in the further development of the earth, such as balancing CO2 and O2 and other gasses in the atmosphere, or perhaps bacteria creating oil resevoirs as a form of planetary lubricant to deal with the internal stresses caused by the start of plate tectonics.

I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.[/i]


dhw: And how do you propose to test the fundamental function performed by the millions of life forms (root types and their variants) that have disappeared?


david Evolution implies replacement and in the case of evolution from simple to more complex

Start by testing the ones that are currently living. How does their lives, input and output, impact the environment.

--
Without darkness there can be no light, no truth without lies.

Genome complexity; epigenetics: Lamarck is back

by David Turell @, Sunday, September 02, 2018, 15:12 (23 days ago) @ Balance_Maintained

.


TONY: In the end, we will find periodic creation of flora and fauna in limited branches at the cusp of great atmospheric or geologic changes in which the arriving types play a significant roll in the further development of the earth, such as balancing CO2 and O2 and other gasses in the atmosphere, or perhaps bacteria creating oil resevoirs as a form of planetary lubricant to deal with the internal stresses caused by the start of plate tectonics.

I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.[/i]


dhw: And how do you propose to test the fundamental function performed by the millions of life forms (root types and their variants) that have disappeared?


david: Evolution implies replacement and in the case of evolution from simple to more complex


David: Start by testing the ones that are currently living. How does their lives, input and output, impact the environment.

I've published here the wolves Yellowstone study of changes down to how it affected river sides vegetation .

Genome complexity; epigenetics: Lamarck is back

by dhw, Sunday, September 02, 2018, 09:17 (23 days ago) @ David Turell

TONY: I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.

dhw: And how do you propose to test the fundamental function performed by the millions of life forms (root types and their variants) that have disappeared?

DAVID: Evolution implies replacement and in the case of evolution from simple to more complex.

Agreed. How will that enable us to test the fundamental function performed by the millions of life forms that have disappeared?

TONY: Start by testing the ones that are currently living. How does their lives, input and output, impact the environment.

I’ll look forward to your findings, Tony! And I’ll look forward even more to hearing how you plan to test the fundamental function of all the pre-historic organisms that disappeared because their fundamental function was no longer fundamental, and of all the organisms that have disappeared during the modern age.

Genome complexity; epigenetics: Lamarck is back

by David Turell @, Sunday, September 02, 2018, 15:24 (23 days ago) @ dhw

TONY: I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.

dhw: And how do you propose to test the fundamental function performed by the millions of life forms (root types and their variants) that have disappeared?

DAVID: Evolution implies replacement and in the case of evolution from simple to more complex.

Agreed. How will that enable us to test the fundamental function performed by the millions of life forms that have disappeared?

TONY: Start by testing the ones that are currently living. How does their lives, input and output, impact the environment.

dhw: I’ll look forward to your findings, Tony! And I’ll look forward even more to hearing how you plan to test the fundamental function of all the pre-historic organisms that disappeared because their fundamental function was no longer fundamental, and of all the organisms that have disappeared during the modern age.

Already seen in the wolves Yellowstone studies.

Genome complexity; fat control

by David Turell @, Thursday, February 14, 2013, 15:10 (2049 days ago) @ David Turell

Long non-coding RNA (lncRNA) controls the production of fat cells:

http://medicalxpress.com/news/2013-02-noncoding-rnas-fat-cells.html#ajTabs

Genome complexity; gene expression

by David Turell @, Monday, February 18, 2013, 15:58 (2045 days ago) @ David Turell

Long non-coding RNa controls gene expression. Important in fetal development; forms loops with DNA:

http://www.sciencedaily.com/releases/2013/02/130217134240.htm

"To discover how such enhancer-like RNAs function, the Shiekhatter laboratory deleted candidate molecules with known roles in activating gene expression, and assessed if they were related to RNA-dependent activation. They found that depleting components of the protein complex known as Mediator specifically and potently diminished the ability of ncRNA-a to start the process of transcribing a gene into RNA. Further, they found that these activating ncRNAs can attach to Mediator at multiple locations within the Mediator protein complex, and Mediator itself can interact with the enhancer element site on DNA that encodes these activating ncRNAs. Their results also determined how mutations in a protein that makes up the Mediator complex, called MED12, drastically diminishes Mediator's ability to associate with activating ncRNAs."

Yes, complexity

Genome complexity: Helicase speed

by David Turell @, Thursday, February 21, 2013, 05:18 (2042 days ago) @ David Turell

The enzyme that unwinds DNA for replication or manufacture can spin up to 10,000 times a minute.

http://www.evolutionnews.org/2013/02/unwinding_the_d_1069371.html

"DNA helicase travels ahead of the replication fork, continuously opening and unwinding the DNA double helix to provide the template needed by the DNA Polymerase. With a rotational speed of up to 10,000 rotations per minute, the helicase rivals the rotational speed of jet engine turbines.'

Talk about a nanomachine!!

Genome complexity: RNA controls

by David Turell @, Thursday, February 21, 2013, 15:32 (2042 days ago) @ David Turell

Destroying or organizing RNA in a cell is up to the exosome, a conplex set of organic molecules. Exactly how it works is not fully understood, but it exists in all forms of cellular life, conseved at all levels of evolution:

"Any errors that occur during the synthesis of RNA molecules or unwanted accumulation of RNAs can be damaging to the cell. The elimination of defective RNAs or of RNAs that are no longer needed are therefore key steps in the metabolism of a cell. The Exosome, a multi-protein complex, is a key machine that shreds RNA into pieces. In addition, the Exosome also processes certain RNA molecules into their mature form. However, the molecular mechanism of how the Exosome performs these functions has been elusive."

Read more at: http://phys.org/news/2013-02-macromolecular-shredder-rna-unravel-machinery.html#jCp

Genome complexity: a new RNA

by David Turell @, Wednesday, February 27, 2013, 18:30 (2036 days ago) @ David Turell

Circular Rnas, very large, can control micro RNAs and reverse their function. Another very complex layer of gene expression controls.

http://www.nature.com/news/circular-rnas-throw-genetics-for-a-loop-1.12513?WT.ec_id=NAT...

Genome complexity: a new RNA

by David Turell @, Monday, March 04, 2013, 18:12 (2031 days ago) @ David Turell

More info. A whole new level of gene regulation:

http://www.genomeweb.com//node/1199156?hq_e=el&hq_m=1518660&hq_l=1&hq_v=734...

Circular RNA's are in various organs

Genome complexity: a new RNA, circular

by David Turell @, Tuesday, August 01, 2017, 18:35 (420 days ago) @ David Turell

Known about for many years but the function, if any is still unknown:

http://www.the-scientist.com/?articles.view/articleNo/49873/title/Uncovering-Functions-...

"Kadener’s work was published earlier this year,1 back-to-back in Molecular Cell with another group’s study—on human and mouse cells—that had simultaneously come to the same conclusion: translation of circRNAs can and does occur in living cells.2 For now, neither group has any hint of the function of these proteins, or of how common circRNA translation really is, but “you can imagine that it has some biological importance,” Kadener notes. RNA researcher William Jeck, currently a fellow at Harvard Medical School, agrees. Many scientists had “written off translation,” he says. “This is extremely exciting evidence that other circles may produce peptides that may be biologically relevant. . . . It’s really changed the paradigm.”

***

"Now, research on circRNAs is exploding, and the molecules’ biogenesis is gradually becoming clearer. At least two proteins, Muscleblind and Quaking, have been linked to circle formation, which generally occurs when the cell’s splicing machinery connects a downstream splice donor to an upstream splice acceptor, such as joining an exon’s 5´ end to its own 3´ end or an upstream exon’s 3´ end, in a process known as backsplicing. Recently, several additional mechanisms have been proposed (see “Making the Rounds” here), and some circRNAs contain introns, either instead of or in addition to exons. Regardless of their genetic makeup, the lack of ends makes circles less vulnerable to exonuclease enzymes, allowing them to persist in cells for days, unlike their linear counterparts, whose life spans are measured in hours or minutes.

"Despite a growing appreciation for the abundance—and now translation—of circRNAs in eukaryotes, there’s still very little understanding of what exactly circRNAs do. “We don’t even know how much of it is functional,” says Jeremy Wilusz, an RNA researcher at the University of Pennsylvania Perelman School of Medicine. “What’s the point of these circles? Why are they made?”

***

"CircRNAs also appear to associate with proteins, suggesting another suite of potential regulatory functions. For example, researchers recently showed that a circRNA produced by the Foxo3 gene (called circ-Foxo3) interacts with proteins involved in cell proliferation, including a key cyclin-dependent kinase and one of its inhibitors, suggesting a role in the cell cycle. And while most exon-containing circles accumulate in the cytoplasm, those that retain introns are often found in the nucleus, where they encounter proteins involved in transcription. In 2015, scientists in China showed that a group of exon-intron circRNAs promoted transcription of their parent genes via interaction with RNA polymerase II.10 Other studies have shown circles interacting with different RNA-binding proteins as well, including proteins now linked to circRNA biogenesis, such as Muscleblind and Quaking, and Argonaute proteins, well-known for their participation in RNAi-based gene regulation.

***

"Of course, how circRNAs come to be understood in the lab and possibly one day used in the clinic remains to be seen, as the study of these looped molecules represents an area that’s still young. But if the past five years are any indication, the study of circRNAs is rapidly ramping up. “What’s amazing to me is how fast this field has grown,” says Wilusz, whose lab supplies plasmids expressing circRNAs to other research groups and has recorded a dramatic uptick in requests in the last couple of years. “It’s really taking off.”

"Rajewsky, whose group is now focusing on circRNAs’ interactions in the brain, agrees that the best is very much ahead. “We’re really just at the beginning of an exciting journey,” he says. “It doesn’t happen often in molecular biology that you find such a fundamentally new phenomenon.'” 

Comment: So far some hints of gene regulation, but the overall reason for circRNA is still not clear.

Genome complexity:cell controls of gene expression

by David Turell @, Thursday, August 03, 2017, 18:04 (418 days ago) @ David Turell

A new study shows how a newly found RNAi works. It is a giant molecule. Be sure to see the diagrams:

https://phys.org/news/2017-08-view-rnai-effect-repressing-gene.html

"Like other creatures, we humans depend on RNAi to fine-tune the expression of our genes. We could not survive without it.

"Today in Molecular Cell, a team led by structural biologist Leemor Joshua-Tor, an HHMI Investigator and professor at Cold Spring Harbor Laboratory (CSHL), publishes atomic-resolution pictures and a comprehensive analysis of the workings of a part of the RNAi machinery. Although much is already known about this machinery, important mysteries about its function have remained unsolved.

"The new discoveries pertain to the way several parts of the machinery come together and work in concert to tamp down gene expression. They can do this in various ways, but the new pictures are about one way in particular: events occurring after the attachment of the machinery to an RNA message (mRNA) copied from a gene. This association of the RNAi machinery and a gene's message is prelude to destruction of the message before it arrives at a cellular protein factory called the ribosome. When the machinery works properly in this mode, the protein never gets made.

"The primary component of the RNAi machinery is called RISC - the RNA-induced silencing complex. It contains two essential parts, a small RNA molecule called a microRNA (miRNA) which guides RISC to its mRNA target; and a much larger component into which the guide RNA fits, a protein called Argonaute, which, Joshua-Tor showed in 2004, actually performs the "slicing up" of the mRNA.

"Now Joshua-Tor's team has succeeded in showing how in humans, a protein called GW182 physically associates with RISC. It was known that there are three possible binding sites on GW182 for Argonaute. An atomic level view of one, called a hook motif, reveals a gate-like interaction. The pictures show that human Argonaute has a single binding site for GW182, and that binding of the guide sequence increases the affinity of the Argonaute and GW182.

"Showing that human GW182 can "multivalently" recruit up to three copies of Argonaute at once, experimenters in the lab led by first author Elad Elkayam suggest a possible source of synergy. "There may be greater efficiency in destroying the mRNA target, we speculate, because of 'crosstalk' between the RISC complexes and GW182," Joshua-Tor says."

Comment: This giant molecule is vital for life to control gene expression. It certainly looks designed, and I think it was.

Genome complexity: origins of DNA folding

by David Turell @, Friday, August 11, 2017, 00:23 (411 days ago) @ David Turell

Apparently all the way back to Archaea:

https://phys.org/news/2017-08-dna-archaea.html

"The archaeal DNA folding, described today in the journal Science, hints at the evolutionary origins of genome folding, a process that involves bending DNA and one that is remarkably conserved across all eukaryotes (organisms that have a defined nucleus surrounded by a membrane).

"Like Eukarya and Bacteria, Arachaea represent one of the three domains of life. But Archaea are thought to include the closest living relatives to an ancient ancestor that first hit on the idea of folding DNA.

"Scientists have long known that cells in all eukaryotes, from fish to trees to people, pack DNA in exactly the same way. DNA strands are wound around a 'hockey puck' composed of eight histone proteins, forming what's called a nucleosome. Nucleosomes are strung together on a strand of DNA, forming a "beads on a string" structure. The universal conservation of this genetic necklace raises the question of its origin.

"If all eukaryotes have the same DNA bending style, "then it must have evolved in a common ancestor," said study co-author John Reeve, a microbiologist at Ohio State University. "But what that ancestor was, is a question no one asked."

***

"The researchers revealed that despite using a single type of histone (and not four as do eukaryotes), the archaea were folding DNA in a very familiar way, creating the same sort of bends as those found in eukaryotic nucleosomes.

"But there were differences, too. Instead of individual beads on a string, the archaeal DNA formed a long superhelix, a single, large curve of already twisty DNA strands.
"In Archaea, you have one single building block," Luger said. "There is nothing to stop it. It's almost like it's a continuous nucleosome, really."

"This superhelix formation, it turns out, is important. When CU Boulder postdoctoral researcher Francesca Mattiroli, together with Thomas Santangelo's lab at Colorado State University, created mutations that interfered with this structure, the cells had trouble growing under stressful conditions. What's more, the cells seemed to not be using a set of their genes properly.

"'It's clear with these mutations that they can't form these stretches," Mattiroli said.
The results suggest that the archaeal DNA folding is an early prototype of the eukaryotic nucleosome.

"'I don't think there's any doubt that it's ancestral," Reeve said."

Comment: this is the best sort of evidence that evolution is a process of common descent. Archaea are the oldest of the three domains of life, and closest to original life forms.

Genome complexity: circular DNA in brains

by David Turell @, Friday, August 11, 2017, 04:50 (410 days ago) @ David Turell

It is not clear what they do:

https://phys.org/news/2017-08-circular-rna-linked-brain-function.html

"While hundreds of circular RNAs (circRNAs) are abundant in mammalian brains, one big question has remained unanswered: What are they actually good for?

***

"RNA is much more than the mundane messenger between DNA and the protein it encodes. Indeed, there are several different kinds of non-coding RNA molecules. They can be long non-coding RNAs (lncRNAs) or short regulatory RNAs (miRs); they can interfere with protein production (siRNAs) or help make it possible (tRNAs). In the past 20 years, scientists have discovered some two dozen RNA varieties that form intricate networks within the molecular microcosm. The most enigmatic among them are circRNAs, an unusual class of RNAs whose heads are connected to their tails to form a covalently closed ring. These structures had for decades been dismissed as a rare, exotic RNA species. In fact, the opposite is true. Current RNA-sequencing analyses have revealed that they are a large class of RNA, which is highly expressed in brain tissues.

***

"Intriguingly, most circular RNAs are unusually stable, floating in the cytoplasm for hours and even days on end. The systems biologists proposed that—at least sometimes - circRNAs serve gene regulation. Cdr1as, a large single-stranded RNA loop that is 1,500 nucleotides around, might act as a "sponge" for microRNAs. For example, it offers more than 70 binding sites for a microRNA called miR-7. MicroRNAs are short RNA molecules that typically bind to complementary sequences in messenger RNAs, thereby controlling the amounts of specific proteins produced by cells.

"Additionally, Rajewsky and his collaborators mined databases and discovered thousands of different circRNAs in nematode worms, mice and humans. Most of them were highly conserved throughout evolution. "We had found a parallel universe of unexplored RNAs," says Rajewsky. "Since publication the field has exploded; hundreds of new studies have been carried out."

"For the current paper in Science, the systems biologists teamed up with Carmen Birchmeier's lab at the MDC to reconsider Cdr1as. "This particular circle can be found in excitatory neurons but not in glial cells," says Monika Piwecka, one of the first authors of the paper and coordinator of most of the experiments. "In brain tissues of mice and humans, there are two microRNAs called miR-7 and miR-671 that bind to it." In a next step, Rajewsky and his collaborators selectively deleted the circRNA Cdr1as in mice using the genome editing technology CRISPR/Cas9. In these animals, the expression of most microRNAs in four studied brain regions remained unperturbed. However, miR-7 was downregulated and miR-671 upregulated. These changes were post-transcriptional, consistent with the idea that Cdr1as usually interacts with these microRNAs in the cytoplasm.

***

"The changes in microRNA concentration had dramatic effects on the mRNA and proteins produced by nerve cells, especially for a group called "immediate early genes." They are part of the first wave of responses when stimuli are presented to neurons. Also affected were messenger RNAs that encode proteins involved in the maintenance of the animals' sleep-wake cycles.

***

"'Functionally, our data suggest that Cdr1as and its direct interactions with microRNAs are important for sensorimotor gating and synaptic transmission," says Nikolaus Rajewsky. "More generally, since the brain is an organ with exceptionally high and diverse expression of circular RNAs, we believe that our data suggest the existence of a previously unknown layer of biological functions carried out by these circles.'"

Comment: the genome control gets more and more complex with more layers of control. It could be expected, as complex as the brain is, there are many layers of control over its plasticity.

Genome complexity: circular DNA in brains

by David Turell @, Saturday, August 12, 2017, 01:03 (409 days ago) @ David Turell

More work reported:

http://www.the-scientist.com/?articles.view/articleNo/50061/title/First-In-Vivo-Functio...

"Using mouse and human postmortem brains, the team showed that miR-7, and to a much lesser extent, another microRNA, miR-671, both bind to Cdr1as.

"Then, the researchers employed CRISPR-Cas9 to delete the locus in mice and create Cdr1as-deficient mutants. Although the knockout animals were outwardly normal—they were viable, fertile, and showed no obvious changes in brain anatomy—the team detected altered levels of free microRNA in areas of the brain where Cdr1as would normally have been expressed: miR-671 was slightly upregulated, while miR-7 levels were markedly lowered—a result that could reflect the circle’s role in preventing degradation of this microRNA by binding to it in wild-type animals, Rajewsky notes.

"Because microRNAs play a role in regulating messenger RNA, the researchers next looked for changes in gene expression in Cdr1as-deficient animals. They found that knockout mice showed altered expression of a set of genes associated with brain activity called immediate early genes—several of which have already been identified as targets of miR-7. “It’s known that neuronal activity is often marked by upregulation of immediate early genes,” Rajewsky says. In the brains of knockout mice, “it was very clear that immediate early genes, as a group, go up.”

"Consistent with this change in gene expression, the researchers found on closer inspection that mutant mice did indeed show abnormalities in neuronal activity. Among other things, single-cell analyses of neurons revealed that, compared to controls, knockout mice had more than double the frequency of miniature excitatory postsynaptic currents—a sign of disrupted neurotransmission.

"Finally, the team ran a suite of experiments to look for behavioral consequences of Cdr1as-deficiency. Although knockout mice exhibited normal anxiety levels and no obvious memory defects, the researchers found that the mutants performed poorly in prepulse inhibition experiments, which measure an animal’s ability to suppress a startle response to an aversive stimulus, such as a sudden loud noise, if a preceding, weaker version of the stimulus has already been played as a warning."

Comment: Just adding another layer of genome complexity in the brain. How much complexity must be shown in the layers of the genome before the need for a designer is recognized?

Genome complexity: controlling cell specificity

by David Turell @, Tuesday, August 22, 2017, 22:30 (399 days ago) @ David Turell

All cells have the same starting DNA with an allele from each parent, but not all alleles are expressed in different tissues. "Enhancer" areas in the DNA exert controls over the process of developing different functional tissues:

https://www.sciencedaily.com/releases/2017/08/170818092138.htm

"Every gene in (almost) every cell of the body is present in two variants -- so called alleles: one is deriving from the mother, the other one from the father. In most cases both alleles are active and transcribed by the cells into an RNA message. However, for a few genes, only one allele is expressed, while the other one is silenced. The decision whether the maternal or the paternal version is shut down occurs early in embryonic development -- one reason, why for long it was thought that the pattern of active alleles is nearly homogeneous in the various tissues of the organism.

"The new study (DOI:10.7554/eLife.25125), where CeMM PhD Student Daniel Andergassen is first author, uncovers a different picture. By performing the first comprehensive analysis of all active alleles in 23 different tissues and developmental stages of mice, the team of scientists revealed that each tissue showed a specific distribution of active alleles.

***

"The scientists found that both genetic and epigenetic differences between the maternal and paternal allele contributed to the observed tissue-specific activity patterns. "Our results indicate that a large part of those patterns are induced by so-called 'enhancers'," co-senior author Quanah Hudson, now at IMBA (Institute for molecular Biotechnology of the Austrian Academy of Sciences) explains. "Enhancers are DNA regions that are often located at quite some distance from the observed allele, but nevertheless have a direct influence on their activity."

"'This study reveals for the first time a comprehensive picture of all active alleles in different tissues -- we have uncovered the first complete allelome" Florian Pauler, now at ISTA (Institute of Science and Technology Austria) and co-senior author, adds.

***

"Some of the genes that contributed to the tissue-specific activity patterns were located on the X chromosome and escaped so-called "X-chromosome inactivation," where one of the two X chromosomes in females gets shut down. Previously it was reported that around 3% of X-chromosomal genes in mice and 15% in humans escape inactivation. However, this study revealed that mice are more similar to humans than previously thought, with an average of around 10% of active genes escaping X-inactivation per tissue. By examining a broad range of organs the researchers showed that the number of escapers varies dramatically between tissues.

***

"Finally, the allelome offers a near complete picture of "genomic imprinting," the process that leads to epigenetic silencing of either the maternal or paternal allele that is initiated by an epigenetic mark placed in either the egg or sperm. Previously, it was reported that approximately 100 genes can be subject to imprinted silencing -- but in many cases, the tissue specificity was not known. This study led to the discovery of 18 new imprinted genes, validated some known genes and resolved the disputed status of some others to provide a gold standard list of 93 imprinted genes in mouse. The scientists found that those new genes were located near to other imprinted genes, indicating that they were co -- regulated. Interestingly, this study demonstrated that Igfr2, the first imprinted gene discovered by Denise Barlow in 1991, is surrounding by a large cluster of imprinted genes that extend over 10% of the chromosome, making it the largest co-regulated domain in the genome outside of the X chromosome. Fittingly, after her lab found the first imprinted gene, and discovered the first imprinted non-coding RNA shown to control imprinted silencing."

Comment: DNA doesn't just make protein. It has to use these complex arrangements to specify cells and tissues in production. This is specified complexity, which cannot have happened by chance.

Genome complexity:a protein controls chromosomes

by David Turell @, Friday, August 25, 2017, 00:56 (396 days ago) @ David Turell

A specific protein has been found to control chromosomes and form the nucleus:

https://www.sciencedaily.com/releases/2017/08/170824124708.htm

"A protein that crosslinks the DNA to allow proper nuclear envelope reformation.
Every one of our cells stores its genome within the nucleus -- the quintessential subcellular structure that distinguishes eukaryotic cells from bacteria. When animal cells divide, they disassemble their nucleus, releasing individual chromosomes for proper segregation to daughter cells. At the end of cell division, the daughter cells reassemble a single nucleus around a complete set of chromosomes. The formation of a single nucleus is critical for the maintenance of genomic integrity. Individual chromosomes packaged into separate, small nuclei are prone to massive DNA damage, leading to mutations as well as chromosome rearrangement and loss.....how cells package their genome into just one nucleus has been a mystery.

"The Gerlich lab at the IMBA set out to solve this problem by screening for genes that are required to assemble a single nucleus in human cells. They uncovered "barrier-to-autointegration factor" (BAF), a multifunctional protein that binds DNA as well as many proteins. Without BAF, cells formed fragmented nuclei at the end of cell division. BAF was already known to link DNA to specific proteins at the nuclear membrane. Unexpectedly, Gerlich's lab discovered that nuclear assembly did not require BAF's association with nuclear membrane proteins. Instead, they found that BAF's ability to bind and bridge distant DNA sites was essential to shape a single nucleus.

"How does BAF's association with DNA regulate formation of the nucleus? The authors found that BAF forms a compact and mechanically stiff network with DNA. This created a coherent surface mesh around the set of chromosomes, which is impenetrable for nuclear membranes. This barrier prevents membranes from separately enwrapping individual chromosomes, and therefore guides the formation of a single nucleus.

"The work, published in the current issue of Cell, answers a fundamental question in biology and reveals an entirely unanticipated function for BAF. "Our findings suggest an entirely new role for DNA cross-bridging beyond genomic functions such as regulating gene expression and recombination, by forming boundaries and mechanical scaffolds of subcellular compartments. We are excited to further uncover the molecular mechanisms that shape mitotic chromosomes and control their interactions with other cellular components" says Gerlich."

Comment: Once again we see evidence of careful design. Cells constantly divide and the chromosomes must be carefully reproduced and packaged into a single nucleus. Evolved by chance, no way!

Genome complexity:cell controls of gene expression

by David Turell @, Wednesday, August 30, 2017, 22:56 (391 days ago) @ David Turell

Another control mechanism is discovered:

https://phys.org/news/2017-08-key-factor-gene-silencing.html

"Wang and colleagues describe a key role for a protein called RSF1 in silencing genes. Besides the molecular biology details, the researchers also showed that disruption of RSF1 expression in the embryos of African clawed frogs caused severe developmental defects in the tadpoles—through a dysregulation of mesodermal cell fate specification.

"RSF1 acts on chromatin, the organized structure of the chromosome where the 6-foot-long DNA of each human cell is highly condensed by wrapping around spools of histone proteins. Chromatin is not static, however—it is highly dynamic and changes in its structure to control different physiological processes.

"One contributor to chromatin fluidity is modifications of the histone proteins made by adding or removing chemical groups to the histone tails. The histones can be modified by acetylation, phosphorylation, methylation, ubiquitination or ADP-ribosylation.

"In his current work, Wang, an associate professor of biochemistry and molecular genetics in the UAB School of Medicine, focused on the addition of ubiquitin to the histone subunit H2A. This prevalent modification is linked to gene silencing, and removal of ubiquitin from H2A leads to gene activation. Wang and colleagues discovered that RSF1 mediates the gene-silencing function of ubiquitinated-H2A.

"They found that RSF1—which stands for remodeling and spacing factor 1, a subunit of the RSF complex—is a ubiquitinated-H2A binding protein that reads ubiquitinated-H2A through a previously uncharacterized and obligatory ubiquitinated-H2A binding domain.

"In human and mouse cells, the genes regulated by RSF1 were found to overlap significantly with those controlled by part of a complex that ubiquitinates H2A. Knockout of RSF1 in cells derepressed the genes regulated by RSF1, and this was accompanied by changes in ubiquitinated-H2A chromatin organization and release of linker histone H1.

"In the paper, Wang and colleagues proposed a model for the action of RSF1 in gene silencing.

"'RSF1 binds to ubiquitinated-H2A nucleosomes to establish and maintain the stable ubiquitinated-H2A nucleosome pattern at promoter regions," they wrote. "The stable nucleosome array leads to a chromatin architecture that is refractory to further remodeling required for ubiquitinated-H2A target gene activation. When RSF1 is knocked out, ubiquitinated-H2A nucleosome patterns are disturbed and nucleosomes become less stable, despite the presence of ubiquitinated-H2A. These ubiquitinated-H2A nucleosomes are subjected to chromatin remodeling for gene activation."

"Wang says knowledge of the ubiquitinated-H2A binding site may help in the discovery of other ubiquitinated histone-binding proteins. "

Comment: Ubiquitination does several things:

"The addition of ubiquitin to a substrate protein is called ubiquitination or less frequently ubiquitylation. Ubiquitination affects proteins in many ways: it can mark them for degradation via the proteasome, alter their cellular location, affect their activity, and promote or prevent protein interactions."

https://en.wikipedia.org/wiki/Ubiquitin

The complexity of these molecular controls is truly amazing and highly suggestive of design.

Genome complexity: 3-D DNA packing

by David Turell @, Thursday, September 07, 2017, 05:35 (383 days ago) @ David Turell

It is tightly packed in very short segments. Functional studies sow he following:

https://evolutionnews.org/2017/09/researchers-highlight-logistics-nightmare-facing-chro...

"What O’Shea’s team saw, in both resting and dividing cells, was chromatin whose “beads on a string” did not form any higher-order structure like the theorized 30 or 120 or 320 nanometers. Instead, it formed a semi-flexible chain, which they painstakingly measured as varying continuously along its length between just 5 and 24 nanometers, bending and flexing to achieve different levels of compaction. This suggests that it is chromatin’s packing density, and not some higher-order structure, that determines which areas of the genome are active and which are suppressed.

"We show that chromatin does not need to form discrete higher-order structures to fit in the nucleus,” adds O’Shea. “It’s the packing density that could change and limit the accessibility of chromatin, providing a local and global structural basis through which different combinations of DNA sequences, nucleosome variations and modifications could be integrated in the nucleus to exquisitely fine-tune the functional activity and accessibility of our genomes.”

"An entry in the Oxford Science Blog asks, “How does a cell know which combination of the 20,000 genes it should activate to produce its specific toolkit?” Look in the formerly named junk DNA for clues:

"The answer to this question may be found in the pieces of DNA that lie between our protein-producing genes. Although our cells contain a lot of DNA, only a small part of this is actually composed of genes. We don’t really understand the function of most of this other sequence, but we do know that some of it has a function in regulating the activity of genes. An important class of such regulatory DNA sequences are the enhancers, which act as switches that can turn genes on in the cells where they are required.

"Switches are not junk. To show that they have important functional roles, the team looked at one enhancer called CTCF.

"Researchers have identified key proteins that appear to define and help organise this domain structure. One such protein is called CTCF, which sticks to a specific sequence of DNA that is frequently found at the boundaries of these domains. To explore the function of these CTCF boundaries in more detail and to investigate what role they may play in connecting enhancers to the right genes, our team studied the domain that contains the α-globin genes, which produce the haemoglobin that our red blood cells use to circulate oxygen in our bodies.

"Firstly, as expected from CTCF’s role in defining boundaries, we showed that CTCF boundaries help organise the α-globin genes into a specific domain structure within red blood cells. This allows the enhancers to physically interact with and switch on the α-globin genes in this specific cell type. We then used the gene editing technology of CRISPR/Cas9 to snip out the DNA sequences that normally bind CTCF, and found that the boundaries in these edited cells become blurred and the domain loses its specific shape. The α-globin enhancers now not only activate the α-globin genes, but cross the domain boundaries and switch on genes in the neighbouring domain.

'Cells divide at least a billion times in the average person, usually without any problem.” Nevertheless, rare abnormalities do occur, as in the case with Down syndrome, when the wrong number of chromosomes (aneuploidy) results. ( my bold)

"Using high resolution microscopes to video the inner workings of live human cells, Dr Draviam and her colleagues at the University of Cambridge (UK) and the European Molecular Biology Laboratory in Heidelberg (Germany), discovered that two proteins — Aurora-B kinase and BubR1-bound PP2A phosphatase — act in opposition to each other, adding or removing phosphate groups respectively, to correctly control the attachment of microtubules to the chromosomes.

"Co-author Duccio Conti, who is Dr Draviam’s PhD student, said: “We found that a balance between Aurora-B kinase and BubR1-bound phosphatase is important to maintain correct chromosome numbers in human cells.'”

Comment: Packing DNA in a cell nucleus requires great complex compactification in order to give the right 3-D relationships for genes to be next to switches enhancers for proper expression of the genes. this is how 'Junk DNA' plays a major role, and obviously isn't junk. Obviously required design by God. Note my bold. The level of mistakes must be very small, but like a good designer, God recognized the need for backup corrective mechanisms to cover that possibility.

Genome complexity: 3-D DNA packing

by dhw, Thursday, September 07, 2017, 10:57 (383 days ago) @ David Turell

QUOTE: “'Cells divide at least a billion times in the average person, usually without any problem.” Nevertheless, rare abnormalities do occur, as in the case with Down syndrome, when the wrong number of chromosomes (aneuploidy) results. ( DAVID’s bold)

DAVID: Note my bold. The level of mistakes must be very small, but like a good designer, God recognized the need for backup corrective mechanisms to cover that possibility.

There is no cure for Down’s syndrome.

Genome complexity: 3-D DNA packing

by David Turell @, Thursday, September 07, 2017, 13:50 (383 days ago) @ dhw

QUOTE: “'Cells divide at least a billion times in the average person, usually without any problem.” Nevertheless, rare abnormalities do occur, as in the case with Down syndrome, when the wrong number of chromosomes (aneuploidy) results. ( DAVID’s bold)

DAVID: Note my bold. The level of mistakes must be very small, but like a good designer, God recognized the need for backup corrective mechanisms to cover that possibility.

dhw: There is no cure for Down’s syndrome.

And there are many others, not as well known. What we have been given has never been completely perfect.

Genome complexity: bacterial gene fusion

by David Turell @, Friday, September 08, 2017, 14:06 (382 days ago) @ David Turell

A new study finds it helps with survivability and produces new protein:

https://phys.org/news/2017-09-bacteria-genes-fuse-production-proteins.html

"All organisms must continuously adapt to their environment in order to survive. Such adaptation is brought about by changes in their genetic material. Together with colleagues from New Zealand, Paul Rainey from the Max Planck Institute for Evolutionary Biology in Plön has been studying the emergence of new, better adapted cell types in the laboratory. The researchers have discovered that one mechanism by which bacteria can develop new characteristics is through the fusion of two existing genes. In some of the cells, this resulted in genes coming under the control of a new promoter, resulting in the synthesis of larger quantities of the protein encoded by the gene. In another case, two neighbouring genes fused together. The protein encoded by the resulting gene – composed of parts of the two original genes – has a different localization within the cell. This effect is also known from other organisms, including humans. A gene fusion of this type results in bacterial cells which are better adapted to their environment.

"Changes to the genetic code in existing genes – mutations – can equip an organism with new characteristics. Duplication of genes and the insertion of extra sections of DNA can also increase an organism's adaptability. Over the course of evolution, it is even possible for completely new genes to be created. This involves changes in previously non-functional stretches of DNA, which result in them becoming functional templates for protein synthesis. Another known mechanism of gene creation is the fusion of two genes, resulting in the production of a novel protein.

***

"According to Rainey and his colleagues, mat formation is caused by a variety of mutational changes in genes that regulate di-guanylate cyclase activity. These mutations switch off negative regulators causing the di-guanylate cyclases to assume an active state. When the researchers eliminated pathways subject to negative regulation they discovered a set of previously unknown mutations that caused the wrinkly mat-forming phenotype. In some of these, the di-guanylate cyclase gene had come under the control of a different promoter, resulting in increased di-guanylate cyclase production.

"In some wrinkly cells, however, the activity of this gene was unchanged. Analysis of the mutations in these cells showed that these mutants contained a chimeric gene formed from the di-guanylate cyclase gene and a neighbouring gene. The protein encoded by the latter is normally active in the cell membrane. "There must, therefore, have been a fusion event between two genes encoding proteins which are usually found at different locations within the cell," explains Rainey. The new protein possesses a membrane domain and is embedded in the cell membrane. This activates the protein, resulting in increased cellulose production.

"In other organisms too, proteins produced by gene fusions frequently end up having a different localization within the cell. In humans, for example, the Kua-UEV gene is the result of the fusion of the Kua and UEV genes. The new UEV protein now localizes to internal cell membranes and performs a new function. In humans, 64 percent of gene families for mitochondrial proteins contain a gene for a protein which is active elsewhere in the cell. "Although in our experiments gene fusion events made up only about 0.1 percent of mutations resulting in the wrinkly phenotype, outside the laboratory they may be more common," says Rainey."

Comment: This study supports Shapiro's work on bacteria manipulating their DNA. It does not explain the underlying mechanism which I think is existing informational instructions in the genome.

Genome complexity: waking sleeping ribosomes

by David Turell @, Tuesday, September 12, 2017, 18:31 (378 days ago) @ David Turell

Under stress bacterial ribosomes will become inactive to conserve energy. This is how they are awakened:

https://phys.org/news/2017-09-hibernating-ribosomes.html

"In research published in Proceedings of the National Academy of Sciences (PNAS), Mee-Ngan F. Yap, Ph.D., assistant professor of biochemistry and molecular biology at Saint Louis University, has uncovered the way a bacterial ribosome moves from an inactive to an active form, and how that "wake up call" is key to its survival.

"Often described as a cell's protein factory, ribosomes translate messenger RNA and link amino acids together to form new proteins. Ribosomes catalyze proteins that are essential for all life.

"In bacteria, ribosomes can take an inactive form called hibernating 100S ribosome. Because protein synthesis accounts for more than half of a cell's energy costs, the inactive ribosome form helps bacteria survive under stressful conditions. During limited nutrient access, antibiotic stress, host colonization, adaptation to the dark and biofilm formation, bacteria aim to conserve energy by shutting down the protein factory.

"Scientists have observed that the hibernating form of the ribosome is not a permanent state and that if conditions are favorable, it can "wake up" and return to its active form, called 70S, and begin to initiate new cycles of protein synthesis.

"'The 100S form is not held together forever," Yap said. "However, until now, the disassociation of 100S ribosome has been a complete black box. We haven't known how ribosomes move from one form to the other."

"Yap was looking for the protein factor that caused the 100S form to return to the intermediate 30S and 50S forms and subsequently into the active 70S form. Studying Staphylococcus aureus, commonly known as staph, Yap found that a GTP hydrolase enzyme called HflX is the wake-up call that will re-activate the ribosome.

"'HflX is one way to break up the 100S ribosome structure so that it can return to the active 70S form," Yap said.

"HflX GTPases are a family of enzymes that are evolutionarily conserved proteins, meaning they also exist in plants, humans and other bacteria. Yap is intrigued by this finding, because while there has been virtually no study of the protein in human cells, it appears in genetic sequencing mapped to cancer patients and those with neurological symptoms, including tic disorder-like syndromes. Scientists do not yet know what this connection means."

Comment: Logically, this entire protection system had to be developed in one step, the sleep and wake-up process available from the onset. It requires foresight and design from a planning mind.

Genome complexity: DNA repair two ways

by David Turell @, Thursday, September 21, 2017, 17:27 (369 days ago) @ David Turell

There is a slow and a fast repair:

http://www.salk.edu/news-release/right-way-repair-dna/

Is it better to do a task quickly and make mistakes, or to do it slowly but perfectly? When it comes to deciding how to fix breaks in DNA, cells face the same choice between two major repair pathways. The decision matters, because the wrong choice could cause even more DNA damage and lead to cancer.

Salk Institute scientists found that a tiny protein called CYREN helps cells choose the right pathway at the right time, clarifying a longstanding mystery about DNA repair.

***

Double-strand breaks, the most serious injuries that happen to DNA, can be repaired by one of two pathways: a fast but error-prone process known as NHEJ (non-homologous end joining) and a slower, error-free pathway known as HR (homologous recombination). The faster pathway efficiently rejoins broken strands, but in the case of multiple breaks it can join the wrong two ends together, making things much worse for a cell. The slower pathway is error-free because it relies on having an undamaged DNA sequence to guide the repair, but this means it can only operate after a cell has copied its genetic information in order to divide. Given that, the fast pathway operates exclusively before DNA is copied, though its machinery is so efficient and prolific that scientists have wondered why it doesn’t outcompete the slower, more-exact pathway after copying, too. Scientists have long suspected that something must be holding the faster option back in those cases.

That something, the new work reveals, is a microprotein called CYREN, which inhibits the faster pathway when a DNA copy is available for the slower pathway to use. CYREN was discovered by another Salk scientist, Alan Saghatelian, as part of a 2015 effort to identify small proteins called “short ORF-encoded peptides” or SEPs, which are increasingly being found to have critical biological roles.

***

The Salk team ... found that with CYREN present, no repairs occurred after the cell copies its DNA, suggesting that it does flip off the master switch, Ku. Without CYREN around, Ku’s fast pathway was active both before DNA was copied and after.

***

These experiments revealed that CYREN directly attaches to Ku to inhibit the fast pathway both depending on timing (before or after DNA copying) and the type of DNA break (smooth versus jagged, for example). Its activity can even tune the ratio of fast to slow repairs.

“Our study shows that CYREN is an important regulator of DNA-repair-pathway choice,” says Karlseder, who holds the Donald and Darlene Shiley Chair at Salk.

Comment: accurate DNA repair is essential for life to continue to exist in proper forms. Dividing cells do make decisions as this research shows, safely going slow when DNA is well organized. This is obviously an automatic system which depends on the status of DNA organization. Too complex to be developed by chance.

Genome complexity: 3-D DNA football controls

by David Turell @, Wednesday, September 27, 2017, 14:56 (363 days ago) @ David Turell

Very sophisticated molecular techniques have found controlling 'footballs' of transcription factors that fit in tightly packed DNA to speed reaction times:

https://phys.org/news/2017-09-scientists-genes-nano-footballs.html

"Crucially, they discovered that transcription factors operate not as single molecules as was previously thought, but as a spherical football-like cluster of around seven to ten molecules of roughly 30 nanometres in diameter.

***

"'We had no idea that we would discover that transcription factors operated in this clustered way. The textbooks all suggested that single molecules were used to switch genes on and off, not these crazy nano footballs that we observed."

"The team believe the clustering process is due to an ingenious strategy of the cell to allow transcription factors to reach their target genes as quickly as possible.

"Professor Leake said: "We found out that the size of these nano footballs is a remarkably close match to the gaps between DNA when it is scrunched up inside a cell. As the DNA inside a nucleus is really squeezed in, you get little gaps between separate strands of DNA which are like the mesh in a fishing net. The size of this mesh is really close to the size of the nano footballs we see.

"'This means that nano footballs can roll along segments of DNA but then hop to another nearby segment. This allows the nano football to find the specific gene it controls much more quickly than if no nano hopping was possible. In other words, cells can respond as quickly as possible to signals from the outside, which is an enormous advantage in the fight for survival.'"

Comment: Life's processes run at very high speed. This 3-D arrangement is logical planning to help get that speed. This must be designed from the beginning of life, or we must assume life ran very slowly at the start.

Genome complexity:3-D DNA neighborhood controls

by David Turell @, Friday, September 29, 2017, 18:59 (361 days ago) @ David Turell

By keeping neighborhoods together as DNA is coiled gene networks can continue to cooperate in a faster fashion:

https://phys.org/news/2017-09-molecular-motor-chromosomes.html

"A molecular "motor" that organizes the genome into distinct neighborhoods by forming loops of DNA has been characterized by researchers at MIT and the Pasteur Institute in France.

"In a study published in 2016, a team led by Leonid Mirny, a professor of physics in MIT's Institute for Medical Engineering and Sciences, proposed that molecular motors transform chromosomes from a loosely tangled state into a dynamic series of expanding loops.

"The process, known as loop extrusion, is thought to bring regulatory elements together with the genes they control. The team also suggested that DNA is decorated with barriers—akin to stop signs—that limit the process of extrusion.

"In this way, loop extrusion divides chromosomes into separate regulatory neighborhoods, known as topologically associating domains (TADs).

***

"Now, in a paper published in the journal Nature, a team led by Mirny and Francois Spitz at the Pasteur Institute, have demonstrated that cohesin does indeed play the role of a motor in the loop extrusion process.

"'Each of these machines lands on the DNA and starts extruding loops, but there are boundaries on DNA that these motors cannot get through," Mirny says. "So as a result of this motor activity, the genome is organized into many dynamic loops that do not cross the boundaries, so the genome becomes divided into a series of neighborhoods."

"The researchers also discovered that a different mechanism, that does not use cohesin, is at work organizing active and inactive regions of DNA into separate compartments in the cell's nucleus.

***

"The team believes the cohesin motors allow each gene to reach out to its regulatory elements, which control whether genes should be switched on or off.

"What's more, it appears that the cohesin motors are stopped by another protein, CTCF, which demarcates the boundaries of each neighborhood. In a recent study in the journal Cell, the Mirny lab, in collaboration with researchers at the University of California at San Francisco and the University of Massachusetts Medical School has demonstrated that if this demarcating protein is removed, the borders between neighborhoods disappear, allowing genes in one neighborhood to talk to regulatory elements they should not be talking to in another neighborhood, and leading to misregulation of genes in the cell.

"'Cohesin is central for gene regulation, and we emphasize that this is a motor function, so it is not just that they (genes and their regulatory elements) find each other somewhere randomly in space, but they were brought together by this motor activity," Mirny says.

***

"'In this work the Mirny and Spitz labs combine mouse models with genomic approaches to study chromosome folding to reveal that the machine that loads the cohesin complex is critical for TAD formation," Dekker says. "From this and another previous study, a molecular mechanism is coming into view where TADs form by cohesin and Nipbl-dependent chromatin loop extrusion, which is blocked by sites bound by CTCF."

"The researchers are now attempting to characterize how the absence of the molecular motor would affect gene regulation. They are also carrying out computer simulations in a bid to determine how the cohesin-based loop extrusion takes place at the same time as the genome is undergoing the independent process of segregating into active and inactive compartments."

Comment: Note the tight controls of the 3-D DNA relationships. Such complexity cannot have been developed step by step. The 3-D relationships allow living cells to reproduce at high speed and to do so accurately by genes and controls being kept close to each other. Only a planning mind can create such a mechanism. Evidence that God exists.

Genome complexity:4-D DNA neighborhood controls

by David Turell @, Friday, October 06, 2017, 22:04 (354 days ago) @ David Turell

Studies now are looking at DNA changes with time:

https://phys.org/news/2017-10-human-genome-d.html

"For decades, researchers have suspected that when a human cell responds to a stimulus, DNA elements that lie far apart in the genome quickly find one another, forming loops along the chromosome. By rearranging these DNA elements in space, the cell is able to change which genes are active.


***

"To track the folding process over time, the research team began by disrupting cohesin, a ring-shaped protein complex that was located at the boundaries of nearly all known loops. In 2015, the team proposed that cohesin creates DNA loops in the cell nucleus by a process of extrusion.

"'Extrusion works like the strap-length adjustor on a backpack," explained Dr. Erez Lieberman Aiden, director of the Center for Genome Architecture at Baylor College of Medicine and senior author on the new study. "When you feed the strap through either side, it forms a loop. DNA seems to be doing the same thing – except that cohesin rings appear to play the role of the adjustor."

"Aiden said a crucial prediction of the 2015 model is that all the loops should disappear in the absence of cohesin. In the new research, Aiden, Rao and colleagues tested that assumption.

"'We found that when we disrupted cohesin, thousands of loops disappeared," said Rao, a medical student at Stanford University, Hertz Fellow and member of the Aiden lab. "Then, when we put cohesin back, all those loops came back – often in a matter of minutes. This is precisely what you would predict from the extrusion model, and it suggests that the speed at which cohesin moves along DNA is among the fastest for any known human protein."

"But not everything happened as the researchers expected. In some cases, loops did the exact opposite of what the researchers anticipated.

"'As we watched thousands of loops across the genome get weaker, we noticed a funny pattern," said Aiden, also a McNair Scholar, Hertz Fellow and a senior investigator at Rice University's Center for Theoretical Biological Physics. "There were a few odd loops that were actually becoming stronger. Then, as we put cohesin back, most loops recovered fully – but these odd loops again did the opposite – they disappeared!"

"By scrutinizing how the maps changed over time, the team realized that extrusion was not the only mechanism bringing DNA elements together. A second mechanism, called compartmentalization, did not involve cohesin.

"'The second mechanism we observed is quite different from extrusion," explained Rao. "Extrusion tends to bring DNA elements together two at a time, and only if they lie on the same chromosome. This other mechanism can connect big groups of elements to one another, even if they lie on different chromosomes. And it seems to be just as fast as extrusion."

"Broad Institute Director Eric Lander, a study co-author, said, "We're beginning to understand the rules by which DNA elements come together in the nucleus. Now that we can track the elements as they move over time, the underlying mechanisms are starting to become clearer.'"

Comment: The fact that DNA can rearrange itself so quickly to respond as necessary indicates there are chemical controls that are yet to be understood. It looks as if DNA can think, but that is beyond possibility. The complexity of the underlying organization it presents demands that the system is designed. Not by chance.

Genome complexity: DNA epigenetic controls

by David Turell @, Monday, October 30, 2017, 17:44 (330 days ago) @ David Turell

Switching DNA genes on and off is conducted by epigenetic mechanisms:

https://www.sciencedaily.com/releases/2017/10/171030095704.htm

"DNA contains the blueprint of an entire organism. Based on the information in this blueprint, every cell knows what it must become and what function it must perform. Throughout the entire lifespan of an organism, the genetic information has to be read correctly to ensure that genes are active at the right time and in the right cells. If these processes are defective, cells acquire the wrong identity -- which can ultimately lead to cancer.

"However, the program that determines which genes are switched on or off as a cell develops does not depend solely on DNA, but is also determined by epigenetic marks. Methylation marks on DNA act as a molecular switch that regulate gene activity in order to coordinate the cell's specialization within the organism.

***

"Tuncay Baubec, professor at the Department of Molecular Mechanisms of Disease at the University of Zurich, and his team have shown that one particular protein plays an important part in this process: The DNA methyltransferase 3A (DNMT3A) enzyme is responsible for positioning the methylation to the right place on the DNA. "DNMT3A places itself preferably in close vicinity to genes that play an important role for development and makes sure that the DNA methylation around these genes is maintained," explains Massimiliano Manzo, lead author of the study. "The DNA methylation around these genes works like a container that ensures that H3K27me3, another epigenetic modification, which normally regulates these genes, is positioned correctly." This means that these essential genes are regulated by two epigenetic layers."

Comment: Once again we see the discovery of giant enzyme molecules in charge of DNA expression. Current Darwin theories do not describe how such large specialized molecules are found in the process of evolution. A designer is required.

Genome complexity: DNA enzyme controls

by David Turell @, Monday, October 30, 2017, 18:01 (330 days ago) @ David Turell

Another enzyme molecule is analyzed which controls DNA expression. see the article to see how complex these enzymes can be:

https://phys.org/news/2017-10-scientists-unveil-protein-critical-gene.html

"The study, led by Dr Lori Passmore opens in new window from the MRC Laboratory of Molecular Biology, is the first to reveal the structure of an important part of the protein, called cleavage and polyadenylation factor (CPF).

"CPF is a complex enzyme made up of many subunits. Cryo-electron microscopy has revolutionised scientists' ability to discover the structure of large, flexible and complex proteins like this in their natural form.

"Dr Lori Passmore, senior author on the paper and group leader at the MRC LMB, said: "Understanding the structure and function of intact CPF, and how it is assembled, has been a central question in the field of gene expression for decades – it's such a fundamental protein but we still don't understand how it works. This was a huge technical challenge because very few structures have been built entirely from scratch using cryo-EM data. We were very excited to finally build the first atomic model of the structure of part of CPF."

"Gene expression - turning the instructions encoded in DNA into proteins - requires a number of important steps. Enzymes copy the gene and produce a single-stranded version of the DNA, called messenger RNA (mRNA).

"The mRNA can travel out of the nucleus of the cell, where the DNA is housed, to the cytoplasm where cellular machinery uses the mRNA's instructions to assemble a protein.
The CPF enzyme is a necessary part of this process – it adds a long string of adenosine molecules, called a 'poly-A tail', to the end of each new mRNA.

"This tail is important because the length of the tail specifies the amount of time that the mRNA is present in the cell, and how often it is translated into proteins. The poly-A tail is also necessary for the mRNA to be transported out of the nucleus.

"Viral infections, such as influenza, target CPF within the cell and disrupt gene expression. The researchers identified a site on CPF where a protein from the virus can bind in a way that may block CPF from interacting with mRNA, and thereby halt gene expression in the cell to the virus' advantage.

"The scientists say this structure will also help them to better understand how CPF works and how defects in poly-A tail addition contribute to diseases - including β-thalassemia, thrombophilia, and cancer."

Comment: Be sure to look at the structure. A blind Darwinian process cannot invent this sort of protein. Designer required.

Genome complexity: Archaea and nuclei

by David Turell @, Wednesday, November 08, 2017, 17:32 (321 days ago) @ David Turell

Eukaryotes have nuclei requiring packing proteins to handle long DNA. Related proteins are found in Archaea:

https://phys.org/news/2017-11-human-cells-hardy-microbes-common.html

"Santangelo, associate professor in the Department of Biochemistry and Molecular Biology, was on a team that found striking parallels between how archaeal cells and more complex cells, including humans' and animals', package and store their genetic material. The breakthrough study, published in Science earlier this year, provided evidence that archaea and eukaryotic cells share a common mechanism to compact, organize and structure their genomes.

***

"Science paper collaborator John Reeve had discovered in the 1990s that histone proteins were not limited to eukaryotes, but were also found in nucleus-free archaea cells. Reeves and Luger began a collaboration to crystallize histone-based archaeal chromatin and compare that structure with eukaryotic chromatin.

"After years of stops and starts and trouble growing reliable archaeal histone crystals – Luger called it a "gnarly crystallographic problem" – the scientists succeeded in resolving the structure of archaeal chromatin, revealing its structural similarity to eukaryotes.

***

"A little high school biology review: Eukaryotes are cells with a nucleus and membrane-bound organelles, and they include fungal, plant and animal – including human – cells. They're set apart from their less complex counterparts, prokaryotes, by the absence of a nucleus. While archaea and bacteria are both prokaryotes, they are only distantly related. Archaea are the likely progenitors of eukaryotes and share many of the same proteins that control gene expression.

"One of life's most fundamental processes – the mechanics by which DNA bends, folds and crams itself into a cell nucleus – is common across all eukaryotes, from microscopic protists to plants to humans.

"Packed inside the nucleus of every eukaryotic cell is several feet of genetic material that is compacted in a very specific way. Small sections of DNA are wrapped, like thread around a spool, roughly two times around eight small proteins called histones. This entire DNA-histone complex is called a nucleosome, and a string of compacted nucleosomes is called chromatin."

Comment: More evidence for pre-planning the future of evolution, just like a change in monkey lumbar changes.


Read more at: https://phys.org/news/2017-11-human-cells-hardy-microbes-common.html#jCp

Genome complexity: DNA is all sizes

by David Turell @, Friday, November 10, 2017, 23:03 (319 days ago) @ David Turell

Looking at all organisms, DNA comes in all sizes totally unexplained:

https://www.quantamagazine.org/shrinking-bat-dna-and-elastic-genomes-20170801/


'Take an onion. Slice it very thin. Thinner than paper thin: single-cell thin. Then dip a slice in a succession of chemical baths cooked up to stain DNA. The dyed strands should appear in radiant magenta — ­the fingerprints of life’s instructions as vivid as rose petals on a marital bed. Now you can count how much DNA there is in each cell. It’s simply a matter of volume and density. A computer can flash the answer in seconds: 17 picograms. That’s about 16 billion base pairs — the molecular links of a DNA chain.


'Maybe that number doesn’t mean much to you. Or maybe you’re scratching your head, recalling that your own hereditary blueprint weighs in at only 3 billion base pairs. “Huh?” joked Ilia Leitch, an evolutionary biologist at the Royal Botanic Gardens, Kew, in England. Her reaction mimicked the befuddlement of countless anthropocentric minds who have puzzled over this discrepancy since scientists began comparing species’ genomes more than 70 years ago. “Why would an onion have five times more DNA than we have? Are they five times more clever?”


'Of course, it wasn’t just the onion that upended assumptions about a link between an organism’s complexity and the heft of its genetic code. In the first broad survey of animal genome sizes, published in 1951, Arthur Mirsky and Hans Ris —pioneers in molecular biology and electron microscopy, respectively — reported with disbelief that the snakelike salamander Amphiuma contains 70 times as much DNA as a chicken, “a far more highly developed animal.” The decades that followed brought more surprises: flying birds with smaller genomes than grasshoppers; primitive lungfish with bigger genomes than mammals; flowering plants with 50 times less DNA than humans, and flowering plants with 50 times more; single-celled protozoans with some of the largest known genomes of all.

***


'Mammals are not especially diverse when it comes to genome size. In many animal groups, such as insects and amphibians, genomes vary more than a hundredfold. By contrast, the largest genome in mammals (in the red viscacha rat) is only five times as big as the smallest (in the bent-wing bat). Many researchers took this to mean that mammalian genomes just don’t have much going on. As Susumu Ohno, the noted geneticist and expert in molecular evolution, put it in 1969: “In this respect, evolution of mammals is not very interesting.”

***


'Or perhaps genomes are unpredictable in the same way life is unpredictable — with exceptions to every rule. “Biological systems are like Rube Goldberg machines,” said Jeff Bennetzen, a plant geneticist at the University of Georgia. “If something works, it will be done, but it can be done in the most absurd, complicated, multistep way. This creates novelty. It also creates the potential for that novelty to change in a million different ways.'”

Comment: I've skipped all the theorizing about why sizes are what they are. There is no coherent theory. Transposons play a key role:

"By then, scientists had learned that B chromosomes are only a tiny fraction of the molecular parasites making genomes fat. The most prolific freeloaders are mobile strings of DNA called transposons, identified in 1944 by Barbara McClintock, the groundbreaking cytogeneticist who was honored with a Nobel Prize for that discovery. Transposons are popularly known as “jumping genes,” although they are rarely in fact true genes. They can get passed down from one generation to the next or transmitted between species, like viruses, and they come in several flavors. Some encode enzymes that snip a transposon out of its place in a genome and paste it elsewhere. Others copy themselves by manufacturing RNA templates or stealing enzymes from other transposons." (plucked out of the article)

Genome complexity: amazing translation efficiency

by David Turell @, Friday, November 17, 2017, 15:09 (312 days ago) @ David Turell

Information in the genome must be translated into proteins and functions. It turns out to be amazingly efficient as compared to computer energy use:

https://phys.org/news/2017-11-astonishing-efficiency-life.html

"All life on earth performs computations – and all computations require energy. From single-celled amoeba to multicellular organisms like humans, one of the most basic biological computations common across life is translation: processing information from a genome and writing that into proteins.

"Translation, it turns out, is highly efficient.

***

"To discover just how efficient translation is, the researchers started with Landauer's Bound. This is a principle of thermodynamics establishing the minimum amount of energy that any physical process needs to perform a computation.

"'What we found is that biological translation is roughly 20 times less efficient than the absolute lower physical bound," says lead author Christopher Kempes, an SFI Omidyar Fellow. "And that's about 100,000 times more efficient than a computer." DNA replication, another basic computation common across life, is about 165 times worse than Landauer's Bound. "That's not as efficient as biological translation, but still stunningly good compared to computers."

"Scaling up to calculate the thermodynamic efficiency of higher-level biological computations like thought, and to understand how important efficiency is to natural selection, offer challenging questions for further research."

Comment: Life maintains its homeostasis through the genome. Limiting the energy required helps life survive its requirement for a constant energy addition. When life originated it is unlikely the process stumbled into this efficiency by chance. It was designed.

Genome complexity:3-D DNA

by David Turell @, Monday, April 23, 2018, 18:16 (155 days ago) @ David Turell

Comes in five different forms when DNA is active in cells:

https://cosmosmagazine.com/biology/helix-no-more-researchers-find-a-new-dna-shape

"A team of Australian researchers at Sydney’s Garvan Institute has identified a knotty version of DNA, known as an I-motif, that appears within DNA when it is actively being read.

***

"According to John Mattick, the out-going director of the Garvan, who was not involved in the research, “This shows another level of dynamic regulation of the DNA code. It’s not just a twisted railway track; it’s got signposts and sidings along the way.”

***

"But over the past couple of decades, mischievous scientists have succeeded in showing that DNA structures other than the elegant helix appear under the microscope. All in all, there are five besides the “standard” shape, known as B-DNA: A-DNA, Z-DNA, triplex DNA, G quadruplex, and I-motif DNA.

***

"To explore whether I-motif DNA existed in living cells, the Garvan team developed an antibody that would bind to it and no other form.

"Injecting the antibody into a variety of cells, the researchers found that the it zeroed in on several targets across the cells – mostly in parts that do not code for proteins – including the regulatory regions that switch genes on and off (known as promotors) and the chromosome tips (called telomeres).

"The I-motif was not detectable all the time. Rather, the antibody, visible because of its green fluorescent tag, came and went as the cells progressed through their cycles of division. However, they were most visible in the late Gap 1 phase, when cells are actively reading their DNA in order to synthesise mRNA and proteins prior to dividing.

“'What excited us most is that we could see the green spots – the I-motifs – appearing and disappearing over time,” says Mahdi Zeraati, the first author of the paper. “It seems likely that they are there to help switch genes on or off.”

"Rather shockingly, the I-motif doesn’t just disobey the structural rules, it also disobeys the normally strict base-pairing rules for DNA, which hold that adenine always binds to thymine, and cytosine always hooks up with guanine. In this instance, the structure is formed by two cytosines pairing up.

"Given that 98% of the genome does not code for proteins, on to decode this information. “Its probably not one dimensional but three or four dimensional”, says Mattick.
As senior author Marcel Dinger puts it, “These findings will set the stage for a whole new push to understand what this new DNA shape is really for.'”

Comment: It is obvious that DNA is much more than a simple linear code, but most of the huge molecule is an active participant in running all phases of life, well beyond simple protein production. Obviously too complex for any chance invention

Genome complexity: DNA repair mechanisms

by David Turell @, Sunday, September 02, 2018, 18:20 (23 days ago) @ David Turell

Without accurate repair mechanisms DNA can become cancer or defects which cause disease conditions:

https://www.sciencedaily.com/releases/2018/09/180901110632.htm

"Researchers from Tokyo Metropolitan University and the FIRC Institute of Molecular Oncology (IFOM) in Italy have uncovered a previously unknown function of the DDX11 helicase enzyme. Mutations in the gene which codes for DDX11 are known to be implicated in Warsaw Breakage Syndrome. They showed that DDX11 plays an important role in DNA repair, and functions as a backup to the Fanconi Anemia (FA) pathway, whose malfunction is associated with another life-debilitating condition.

"DNA plays a central role in the biological function of the cell, but it is constantly being damaged, both spontaneously and through environmental factors. Failure to successfully repair these lesions can lead to malignant tumors or cancer.

***

"Warsaw Breakage Syndrome (WABS) is a genetic disorder; afflicted individuals suffer from mild to severe intellectual disability and growth impairment amongst other potential abnormalities. It was known that mutations in the DDX11 gene in Chromosome 12 in the human genome and the enzyme it codes for, the DDX11 helicase, were responsible for the onset of WABS, yet the mechanism by which DDX11 acted remained unclear.

***

"What they found was that DDX11 played a vital role in DNA repair, acting together with the 9-1-1 checkpoint complex protein, which, as the name suggests, checks the integrity of DNA strands after replication. In doing so, DDX11 is critical in the repair of a wide-range of bulky lesions and also serves as a backup to the so-called FA pathway, specialized in the repair of interstrand crosslinks (ICLs), a harmful type of lesion that can lead to cell death and developmental problems. This finding explains the apparent similarity between WABS and FA cells exposed to ICLs, which caused WABS to be classified as a FA-like disorder. The researchers also discovered that DDX11 is involved in immunoglobulin-variable gene diversification, a key mechanism in the healthy function and adaptability of a healthy immune system. As immunoglobulin-variable gene diversification is induced by abasic sites, the most common endogenous lesion in mammalian cells, one implication is that DDX11 and 9-1-1 promote DNA damage tolerance of abasic sites, a finding that potentially explains the essential role of DDX11 and its similarity with 9-1-1 during development.

"Besides shedding light on the mechanism underlying WABS, the study advances our understanding of the biological mechanisms behind genomic stability and how disorders arise at the cellular level. These results have profound medical significance for several conditions, including cancer and developmental disorders associated with DNA repair deficiency."

Comment: We recognize the complexity of DNA itself. In their own way the enzymes that repair DNA are equally complex given their enormous size as protein molecules. It is obvious that when DNA appeared, these repair enzymes had to be in place or life would not have continued as it has. Only planned design fits this scenario.

Genome complexity: 3 types of bees from one DNA

by David Turell @, Wednesday, September 12, 2018, 15:11 (13 days ago) @ David Turell

A study of the modifications which seem to control the three types of bees, queens, drones, and workers:

https://www.the-scientist.com/news-opinion/as-bees-specialize--so-does-their-dna-packag...


"The bee genome has a superpower. Not only can the exact same DNA sequence yield three types of insect—worker, drone, and queen—that look and behave very differently, but, in the case of workers, it dictates different sets of behaviors.

"A key to the genome’s versatility seems to be epigenetic changes—chemical tags that, when added or removed from DNA, change the activity of a gene. Previous studies had shown distinct patterns of tags known as methyl groups on the genomes of bees performing different roles within their hives.

"In a study published in Genome Research last month, Paul Hurd, an epigenetics researcher at Queen Mary University of London, and colleagues looked at a different type of epigenetic change: histone modifications. DNA wraps around histones, and chemical modifications to these proteins are thought to affect how available genes are to be transcribed.

"In their new study, the researchers report that queen and worker bees each have characteristic patterns of histone modifications on their genomes, and that these differences emerge very early in development, suggesting they may be key to determining the insects’ fates.

"The very different individuals that arise from hive members’ identical genomes have made the honeybee “one of the most well-known and striking examples of phenotypic plasticity,” says Gene Robinson, a genomicist at the University of Illinois who was not involved in the study. Bees are a model, he says, for “understanding how environmental signals are transduced and then trigger these alternate developmental pathways.”

"Larvae are sent down different developmental pathways from the time of hatching by nurse bees (a type of worker), which tailor the insects’ diets according to their future castes. Worker bees that tend to queen larvae and mature queens make their special food, so-called royal jelly, themselves, and it contains a compound known to directly influence histone modifications, the authors note in their paper.

***

"To investigate their role, the research team collected worker and queen bee eggs and larvae from Apis mellifera hives and sampled the larvae 96 hours after they hatched. The team then analyzed the bee genomes for the positions of three different types of histone modifications.

"At 96 hours, the researchers found, the genomes of future workers and queens already had “striking differences” in their patterns of histone modifications, says Robert Lowe, a computational biologist at Queen Mary University of London and one of the paper’s authors. And the locations of the histones that were modified differently in workers and queens corresponded with the sites of genes that have different expression levels between the two populations.

"The authors suggest that the histone modifications drive differences in gene transcription among bees of different castes, which in turn guide them down different developmental paths."

Comment: This is a complex society, well coordinated in their tasks an efficient hive. It certainly looks designed that way and not evolved with steps over time.

Genome complexity: genes and what they control

by David Turell @, Thursday, September 20, 2018, 23:39 (5 days ago) @ David Turell

We still know much about the genome and how genes relate to functions is really not clear:

https://www.sciencedaily.com/releases/2018/09/180917090856.htm

Ever since the decoding of the human genome in 2003, genetic research has been focused heavily on understanding genes so that they could be read like tea leaves to predict an individual's future and, perhaps, help them stave off disease.

A new USC Dornsife study suggests a reason why that prediction has been so challenging, even for the most-studied diseases and disorders: The relationship between an individual's genes, environment, and traits can significantly change when a single, new mutation is introduced.

"Individuals have genetic and environmental differences that cause these mutations to show different effects, and those make it difficult to predict how mutations will behave, " said Ian Ehrenreich, a lead author and biologist at the USC Dornsife College of Letters, Arts and Sciences. "For example, mutations that break the cell's ability to perform DNA mismatch repair are linked to colorectal cancer, but some individuals that harbor these mutations never develop the disease."

***

A growing number of large-scale, genome-wide association studies have revealed which genes are linked to certain diseases, behaviors or other traits. These studies overlook how interactions between genetic differences, the environment, and new mutations -- what scientists have termed "background effects" -- differ from individual to individual.

***

The authors found that background effects result from many, often environment-specific, interactions between mutations and genetic differences. In fact, most of these interactions involved multiple genetic differences interacting with not only a mutation, but also with each other and the environment.

These findings imply that background effects result from complicated interactions between mutations, pre-existing genetic differences, and the environment.

"In the extreme, we found that that these complicated interactions could influence whether a perfectly healthy cell lived or died after a mutation was introduced," Ehrenreich said.
"The role of genetic and environmental context in shaping the effects of genetic mutations on traits may be significantly underappreciated," he said.

"There is an obvious goal here -- to help people prevent disease or lower their risk," Ehrenreich said. "The challenge is that we don't fully understand how genetics work. These critical experiments in yeast and other model organisms help clarify what we might be missing. An important next step would be to examine whether these conclusions hold true for humans." (my bold)

Comment: We have touched only a thin sliver of how the genome works with only two percent of it coding for protein and 80% actively influencing what goes on. The coiled construction and folding allows for 3-D relationships that defy any simple understanding. We are many years for any full understanding.

Genome complexity: genes and what they control

by Balance_Maintained @, U.S.A., Friday, September 21, 2018, 04:35 (4 days ago) @ David Turell

We still know much about the genome and how genes relate to functions is really not clear:

https://www.sciencedaily.com/releases/2018/09/180917090856.htm

Ever since the decoding of the human genome in 2003, genetic research has been focused heavily on understanding genes so that they could be read like tea leaves to predict an individual's future and, perhaps, help them stave off disease.

A new USC Dornsife study suggests a reason why that prediction has been so challenging, even for the most-studied diseases and disorders: The relationship between an individual's genes, environment, and traits can significantly change when a single, new mutation is introduced.

"Individuals have genetic and environmental differences that cause these mutations to show different effects, and those make it difficult to predict how mutations will behave, " said Ian Ehrenreich, a lead author and biologist at the USC Dornsife College of Letters, Arts and Sciences. "For example, mutations that break the cell's ability to perform DNA mismatch repair are linked to colorectal cancer, but some individuals that harbor these mutations never develop the disease."

***

A growing number of large-scale, genome-wide association studies have revealed which genes are linked to certain diseases, behaviors or other traits. These studies overlook how interactions between genetic differences, the environment, and new mutations -- what scientists have termed "background effects" -- differ from individual to individual.

***

The authors found that background effects result from many, often environment-specific, interactions between mutations and genetic differences. In fact, most of these interactions involved multiple genetic differences interacting with not only a mutation, but also with each other and the environment.

These findings imply that background effects result from complicated interactions between mutations, pre-existing genetic differences, and the environment.

This is precisely what I was talking about with the bees.

--
Without darkness there can be no light, no truth without lies.

Genome complexity; lncRNA

by David Turell @, Friday, April 05, 2013, 18:34 (1999 days ago) @ David Turell

Much rising interest in lncRNA.


"At the time, modifying gene expression using lncRNA was not a common goal. In the early 2000s, most molecular biologists were interested in the 1...2% of the human genome that encodes proteins, which were presumed to be the brokers of biological functions. But with the rise of high-throughput sequencing, researchers learned that far from being without function, much of the rest of the genome was transcribed into non-coding RNA, including 20-nucleotide microRNAs, which suppress genes, and lncRNAs of 100 nucleotides or more.

"Last September, the multi-institution ENCODE project to catalogue human DNA elements (see Nature 489, 46...48; 2012) revealed that three-quarters of the human genome is transcribed into non-coding RNA, and that there may be between 10,000 and 200,000 lncRNAs. Scientists have shown that these can activate gene expression and silence genes, and links with disease have begun to emerge.

"Enthusiasm for lncRNA has replaced much of the science community's scepticism. Molecular biology and biochemistry departments have taken note of a flurry of high-impact manuscripts, and some are hiring scientists to work in the emerging field. Funding is becoming easier to find. And the first biotechnology companies focused on lncRNA have taken root."

http://www.nature.com/naturejobs/science/articles/10.1038/nj7443-127a

Genome complexity; lncRNA

by David Turell @, Thursday, April 25, 2013, 16:11 (1979 days ago) @ David Turell

Genome complexity; lncRNA

by David Turell @, Wednesday, July 10, 2013, 02:51 (1903 days ago) @ David Turell

The lncRNA's seem to work in 3 dimensions. How they arose in such specific locations, and they are preciselty positioned, is theorized but really unknown.:

http://www.darwins-god.blogspot.com/2013/07/heres-new-paper-on-long-non-coding-rna.html

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