There are feedback loop molecules that control stress-related gene changes. These changes revert back to normal when the stress is gone:-
"Stress is unhealthy. The cells use therefore a variety of mechanisms to deal with stress and avert its immediate threat. However, certain stressful situations leave marks that go beyond the immediate response; some even seem to be passed on to the next generation. One school of thought that has gained a lot of attention lately, hypothesizes that the epigenome, chemical modifications on the DNA and on proteins, carries information about external influences such as stress. However, when and how environmental cues trigger changes in the epigenome and thus influence our response has remained largely unknown.-"To investigate how the environment can influence epigenetic processes, FMI Senior group leader Marc Bühler and his group work with fission yeast. In a paper published in Cell Reports, they report the identification of a regulatory circuit that buffers a potentially deleterious epigenetic switch under stressful conditions. The capacity to prevent such an epigenetic change is important to the organism, perhaps because the altered epigenetic state is maintained for many cell divisions, well after the stress has subsided."-
 Read more at: http://phys.org/news/2015-01-cellular-memory-stressful-situations.html#jCp

Not only are there antibody producing cells which are modified with a memory to take on any return of a previous pathogen, there are literally white cells ( not red) which roam the blood stream to chomp up invading bacteria:-http://www.evolutionnews.org/2016/01/defending_the_b102559.html-"Neutrophils are produced in the bone marrow and with maturation move out into the blood. Neutrophils are usually the first immune cells from the blood to come to the field of battle. They are attracted to the war zone by cytokines, which are chemical messengers released from injured tissue and activated mast cells, macrophages, and dendritic cells. The process by which they move into the field of battle and toward invading microbes is called chemotaxis. This involves using specific receptors on their plasma membrane to move toward areas of increasing concentration of these chemicals. It's similar to how a bloodhound moves towards its prey by sensing the increasing concentration of the scent, or a shark to blood. Moreover, the same cells that send out cytokines to attract neutrophils and other immune cells also release chemicals that cause inflammation. Inflammation allows the neutrophils to squeeze through the narrow openings between the cells that line the capillaries into the tissues so they can seek out and destroy the enemy.-"Once inside the tissues and brought toward the invading microbes by chemotaxis, the neutrophils activate by using specific receptors on their plasma membrane to attach to specific chemicals on the surface of the intruder. The activated neutrophil usually engulfs the microbe in a process called phagocytosis . Once the microbe is inside, the neutrophil releases various chemicals and enzymes to kill and literally digest it. Neutrophils also kill microbes by releasing the chemical contents of their granules into the tissues.-***-"After neutrophils do their job, they usually die and are phagocytosed by macrophages. Dead neutrophils make up most of the cellular content of pus. Finally, like all activated immune cells, neutrophils release cytokines to promote inflammation, attract other immune cells to the battlefield, and increase the metabolism, often causing fever. -***- "That means the body makes about one million neutrophils per second! -Furthermore, to maintain this constant production, support cells in the bone marrow release a cytokine called Granulocyte Colony Stimulating Factor (G-CSF), which attaches to specific G-CSF receptors on the stem cells in the bone marrow, stimulating them to develop into neutrophils. -Finally, in response to infection and inflammation, some immune cells also release G-CSF, which can often result in a doubling or even tripling of the amount of neutrophils. So, although neutrophils cannot multiply on their own (like microbes can), in response to infection and inflammation some immune cells stimulate the bone marrow to increase neutrophil production. This increase makes more defenders available that can be sent to the battlefield. It is by the release of these cytokines that the body not only develops a fever, but also raises the white blood cell count (leukocytosis), the two main tell-tale signs of infection.-***-"Evolutionary biologists seek to explain how life came into being but they pay attention predominantly to how it looks, not how it must work within the laws of nature to survive. They may speculate on how neutrophils and the control mechanisms involved in their production must have come into being by chance and the laws of nature alone. But this doesn't take into account that this system is irreducibly complex, requiring cells that can produce G-CSF and ones that have specific G-CSF receptors, so they can be instructed to become neutrophils, and cytokines to allow neutrophils to leave the bloodstream, and with specific receptors move toward their prey."-Comment: As a physician I went from simply accepting evolution created this to realizing that evolution cannot create this as an unguided chance process!

Another study into how T cells recognize foreign material when surrounded by a welter of 'self' proteins:

http://medicalxpress.com/news/2016-11-immune-receptors-amplify-invader-mini-machines.html

"When a receptor on the surface of a T cell—a sentry of the human immune system—senses a single particle from a harmful intruder, it immediately kicks the cell into action, launching a larger immune response. But exactly how the signal from a single receptor, among thousands on each T cell, can be amplified to affect a whole cell has puzzled immunologists for decades.

"Now, Salk scientists have discovered the key to the amplification of an "invader" signal. The T cell receptor that detects the intruder turns into a mini-machine, activating and releasing copy after copy of a protein called ZAP70.

***

"T cells are central in the adaptive immune response, which is the body's ability to recognize pathogens and respond to them. A single T cell's receptors screen thousands of molecules at any given second, but most of them originate from the body's own proteins and have to be ignored as "self." Researchers have struggled to explain how, in the wake of overwhelming "self" signals, a T cell can detect and respond to one or two "invader" signals.

"Lillemeier's lab studied ZAP70, a protein that associates with T cell receptors and becomes activated when the receptors recognize a foreign molecule. To track the activity and location of ZAP70 molecules, the team tagged them with a fluorescent marker while anchoring each T cell receptor in place. To the group's surprise, ZAP70 molecules were being activated by the T cell receptors and then moving away, spreading throughout the cell.

***

"By churning out ZAP70 and sending it throughout the cell—as opposed to just activating a handful of ZAP70s and keeping them tethered to the T cell receptor—the immune cells can rapidly spread a signal throughout the cell.

"'What we saw is that at the beginning of signaling, you have lots of ZAP70 being released from the T cell receptor to amplify and distribute the signal," says Lillemeier. "But once the signaling is established, the T cell receptor actually adapts and stops releasing so much of ZAP70."

"Questions remain on how the process works, including what the ultimate destinations of the ZAP70 molecules are and how they go on to transmit signals. But the observation, Lillemeier says, is progress toward understanding how T cells identify and react to pathogens.

"'It's really important to understand this process since T cells are at the center of the adaptive immune response," he says. "If the receptors are not controlled well, you're sick; you might either have an autoimmune disease or you can't respond to infections." Being able to make the receptors have a stronger or weaker signal—perhaps by changing how much ZAP70 they activate and release—could help treat these kinds of diseases, he adds." (my bold)

Comment: This is an automatic cellular reaction, no thought involved. The researchers are now looking for the feedback mechanism to control the reaction, a must in all the biochemistry of life. Not by chance.

dhw: QUOTE: “Aside from the obvious (and intriguing) challenge of understanding the enormous complexity of life's information payload, evolution purports to explain its origins.”
> 
> I accept all your arguments about continuity etc. but your author here is also doing precisely the same as Dawkins: offering a gross misrepresentation in order to make his case sound more convincing. The theory of evolution does not purport to explain life's origins.-The statement you quote is over reaching I admit, however it is not a distortion, if, as you say, you accept the continuity. First life had to contain the preparations for evolution, thus the continuum. Evolution begins with first life, not just after life arrives, because first life contains the information permitting alterations, that allows for evolution. Of course, any theory of evolution does not explain the origin of life. There is a fine distinction here. We have quarreled about this before. You cannot disconnect origin from evolution.

dhw: Like BBella, I don't understand how conscious energy can be the only thing in existence and yet separate its own simpler unconscious forms. You now have a God who is part conscious and part unconscious.-DAVID: If God invented the universe, and I'm sure He did, it is not conscious. If God invented life, and I'm sure He did, He started with bacteria, and they are not conscious.-But if nothing existed except consciousness, what did consciousness make an unconscious universe from? As regards bacteria, their non-consciousness is a matter of opinion not fact.-DAVID: The universe appears to have been created. It is not conscious, except through us. We have been developed from an inorganic universe, all controlled by the universal mind which manages all development.
dhw: So your universal mind is separate from the unconscious inorganic universe, which it created out of nothing but its consciousness. As a panentheist, you believe this conscious mind is within AND without BBella's ALL THAT IS. So God is/is not within/separate from the inorganic universe, and is/is not conscious/unconscious. I find this a bit confusing. Perhaps theistic panpsychism will play some role in your thinking, but I'll leave you to sort out the convolutions!
DAVID: Your problem, not mine. The inorganic universe with its lately arrived living portion has a universal consciousness, God.-Ah well, I guess that's one way of ending a discussion. 
 
dhw: So faith is required if one is to dismiss all other solutions. 
DAVID: Now you understand! A breakthrough! You of no faith flounder. 
dhw: We only flounder when we see theists and atheists kidding themselves that reason, science and common sense are on their side, when we ourselves are painfully aware - as you now acknowledge so triumphantly - that reason, science and common sense are on nobody's side, and to be a theist or an atheist you must rely on irrational, non-scientific, non-commonsensical faith. Well, this acknowledgement is indeed a breakthrough! 
DAVID: Funny, but I started as an agnostic, looked at the science and found faith. My mind does not work like yours. Not surprising, we all have our own approaches and prejudices.-Very true. If all our minds worked alike, there would be nothing to discuss!

dhw: As always, a powerful case for design. But design of what? A microcosm within a macrocosm? “DNA tells our cells what to do…a mechanism that can recognize…like an individual intelligent agent…try to come up with a way…self-awareness…respond in several ways…” So many of the actions and attributes we associate with intelligence – and yet we are not even aware of them. It’s as if we are inhabited by a colony of ants, each with their own particular role to play, but constantly communicating, adapting, making decisions in the world that is you or me. It’s what some scientists call cellular intelligence.

The design comes from the intelligent information in DNA. The entire design of the organism. The source of that information is what you and I debate.

xxxxxxx

David’s comment: It is becoming recognized that alternate metabolic pathways may be present in many species, as I noted in our previous discussions about bacteria responding to antibiotics (can't find the reference). The species is still one species. It is not a new evolutionary process as the articles headline proclaim.

dhw: May I suggest that if the killifish is able to cope so quickly with different pollutants, what it carries before the sites are polluted is not an alternative metabolic pathway anticipating whatever might happen next, but the ability to process new information and change its genome accordingly – which means it can construct a new metabolic pathway to cope with each new threat.

On the other hand the article clearly suggests there are variable individuals in the species some of whom can handle the pollution and survive. If the fish are living in pollution they might not survive long enough to produce enough generations of offspring with the ability to survive. You are stretching your theory about cellular abilities to adapt on their own at high speed. I'll repeat current scientific thought as in bacteria. Species variation allows some individuals to survive and adapt the species to a new challenge.

dhw: And I would suggest that this applies to all processes of adaptation, though different organisms will have different capacities for change. You are quite right: this is not the same as innovation. It is simply confirmation that the genome can be changed when an organism experiences new conditions.

This is certainly true if new conditions are not severe and allow for several generations of change.

dhw:We don’t know how far the ability for change can extend. Or do you still think your God put each alternative metabolic pathway for all eventualities into the first cells to pass on to the killifish a few thousand million years later?

Many species have variable individuals who can survive changes, nothing more.

xxxxxxx

dhw: Nobody has yet solved the problem of defining species ... But what is really interesting is the variability between individuals. This would explain how common descent works. Changes can only take place in individuals, and individuals are different. So some will respond to environmental change and others won’t. So far we only know of adaptation and non-adaptation (those that can’t respond will die). But it is conceivable that the variation will also apply to innovation. Some organisms may have the wherewithal to invent. In much the same way as some humans are creative, and some are not.

All organisms can adapt to some degree. To invent a new species is a whole different ball game. Darwin theory has no explanation for it.

Electrons running along DNA for repair and to speed replication:

https://phys.org/news/2017-02-electrons-dna-wire-replication.html

"The electron transfer process in DNA occurs very quickly," says O'Brien, lead author of the study, appearing in the February 24 issue of Science. "It makes sense that the cell would utilize this quick-acting pathway to regulate DNA replication, which necessarily is a very rapid process."

"The researchers found their first clue that DNA replication might involve the transport of electrons through the double helix by taking a closer look at the proteins involved. Two of the main players in DNA replication, critical at the start of the process, are the proteins DNA primase and DNA polymerase alpha. DNA primase typically binds to single-stranded, uncoiled DNA to begin the replication process. It creates a "primer" made of RNA to help DNA polymerase alpha start its job of copying the single strand of DNA to create a new segment of double-helical DNA.

***

"DNA primase and DNA polymerase alpha molecules both contain iron-sulfur clusters. Barton and her colleagues previously discovered that these metal clusters are crucial for DNA electron transport in DNA repair. In DNA repair, specific proteins send electrons down the double helix to other DNA-bound repair proteins as a way to "test the line," so to speak, and make sure there are no mutations in the DNA. If there are mutations, the line is essentially broken, alerting the cell that mutations are in need of repair. The iron-sulfur clusters in the DNA repair proteins are responsible for donating and accepting traveling electrons.

***

"Through a series of tests in which mutations were introduced into the DNA primase protein, the researchers showed that this protein needs to be in an oxidized state—which means it has lost electrons—to bind tightly to DNA and participate in DNA electron transport. When the protein is reduced—meaning it has gained electrons—it does not bind tightly to DNA.

"'The electronic state of the iron-sulfur cluster in DNA primase acts like an on/off switch to initiate DNA replication," says O'Brien.

"What's more, the researchers demonstrated that electron transport through DNA plays a role in signaling DNA primase to leave the DNA strand. (Though DNA primase must bind to single-stranded DNA to kick off replication, the process cannot begin in earnest until the protein pops back off the strand).

"The scientists propose that the DNA polymerase alpha protein, which sits on the double helix strand, sends electrons down the strand to DNA primase. DNA primase accepts the electrons, becomes reduced, and lets go of the DNA. This donation and acceptance of electrons is done with the help of the iron-sulfur clusters.

"'You have to get the DNA primase off the DNA quickly—that really starts the whole replication process," says Barton. "It's a hand off of electrons from one cluster to the other through the DNA double helix."

"Many proteins involved in DNA reactions also contain iron-sulfur clusters and may also play roles in DNA electron transport chemistry, Barton says."

Comment: Can the workings of the genome get more complex that is now known. Absolutely. We've just begun to see how complex it is. Not by chance!

Not just methylation but now M1A and M6A and others are found but exact function not clear:

http://www.nature.com/nature/journal/v542/n7642/full/542503a.html

"at least one-quarter of our mRNAs harbour chemical tags — decorations to the A, C, G and U nucleotides — that are invisible to today's sequencing technologies. (Similar chemical tags, called epigenetic markers, are also found on DNA.) Researchers aren't sure what these chemical changes in RNA do, but they're trying to find out.

"A wave of studies over the past five years — many of which focus on a specific RNA mark called N6-methyladenosine (m6A) — have mapped these alterations across transcriptomes and demonstrated their importance to health and disease. But the problem is vast: these marks coat not only mRNA but other RNA transcripts as well, and they cut across all the domains of life and beyond, marking even viruses with their presence.

"The modifications themselves are not new. What has given them meaning and driven epitranscriptomics into the spotlight is the discovery of enzymes that can add, remove and interpret them. In 2010, chemical biologist Chuan He at the University of Chicago, Illinois, proposed that these chemical tags could be reversible and important regulators of gene expression. Not long afterwards, his group demonstrated2 the first eraser of these marks on mRNA, an enzyme called FTO. That discovery meant that m6A wasn't just a passive mark — cells actively controlled it. And this realization came at about the same time that global approaches, harnessing the power of next-generation sequencing, made it possible to map m6A and other modifications across the transcriptome.

***

"Other RNA modifications have also attracted researchers' attention. In 2016, teams led by chemist Chengqi Yi at Peking University in Beijing and by Rechavi and He used antibody-based methods to map N1-methyladenosine (m1A) in mouse and human cell lines and tissues8. Using different approaches to prevent m1A from interfering with reverse transcription, the two teams showed that m1A, which was discovered in total RNA in the early 1960s, is present on mRNA at the position at which the translation machinery initiates protein production. Stress conditions alter the maps, suggesting that they are dynamic.

"The researchers don't yet know what m1A does, but they have a tantalizing clue: most transcripts have only one m1A site, and these seem to be translated more often than those that lack the modification. “This is very exciting — and of course challenging — because we are dealing with a new regulatory mechanism for translation of messenger RNA,” Rechavi says. An antibody that targets m1A is available from MBL International.

***

"Technical hurdles remain, however, as RNA poses challenges not seen in DNA. One is that RNA readily folds in on itself to form loops and knots, so it is highly structured. In its study15, Oxford Nanopore attached RNA to cDNA, which helps 'iron out' the secondary structures and move the RNA through the pore. A second challenge is that RNA degrades more easily than DNA, a problem that may stymie long-read sequencing approaches.

"Yet another challenge, on the data side, is the sheer number of RNA modifications. Recognition of multiple different modifications on the same RNA would require massive training sets to teach the detection software to distinguish one modification from another. Winston Timp, a biomedical engineer at Johns Hopkins University in Baltimore, Maryland, has been using Oxford Nanopore technology to develop new methods for detecting specific DNA modifications. He now plans to move into RNA modifications, developing a training set that will help recognize m6A modifications. “The problem is, we don't know how diverse on a given molecule the modifications are,” he says. “But this is something we can probe. It's an exciting area of research.'”

Comment: We are seeing only the tip of the research iceberg. How much complexity is needed before it is recognized a designer, God, did this.