https://phys.org/news/2025-02-discovery-high-manganese-centers-photosynthesis.html

"In a small manganese oxide cluster, teams from HZB and HU Berlin have discovered a particularly exciting compound: two high-spin manganese centers in two very different oxidation states. This complex is the simplest model of a catalyst that occurs as a slightly larger cluster in natural photosynthesis, where it enables the formation of molecular oxygen. The discovery is considered an important step towards a complete understanding of photosynthesis.

***

"Now, groups at Humboldt-Universität zu Berlin and HZB have discovered the long-sought high-spin manganese (V) center in a small manganese oxide cluster. The cluster contains only five atoms in total and looks very simple: two oxygen atoms form bridges between two manganese atoms, one of which is bound to a third oxygen atom as a terminal ligand.

"'This is the simplest form of a bonding motif that also occurs in natural photosynthesis, which makes this discovery very exciting," says HZB researcher Konstantin Hirsch.

***

"'This discovery is very encouraging and we will now continue our search for high-spin manganese(V) centers in even larger clusters that are closer to the inorganic cluster in natural photosynthesis. We hope that one day we will be able to unlock the secret of how nature produces all the oxygen molecules that surround us and that we breathe every day," says Ablyasova."

Comment: it took highly sophisticated lab work to do it. How do natural mutations achieve such a complex enzyme? Not by chance.

https://www.the-scientist.com/a-beneficial-bacterium-helps-wounds-heal-72382?utm_campai...

"...recently, we've appreciated that there is a wound microbiome—an entire ecosystem that colonizes wounds and can influence wound healing.”

"Highlighting this, White and her colleagues have shown that a bacterium found in chronic wounds can aid wound healing in mice.4 The results, published in Science Advances, uncover a mechanism of bacterial-driven wound repair and provide a foundation to develop microbiome-based therapies.

“'This study is unique in terms of bringing light on the good part of the chronic wound microbiome,” said Irena Pastar, who researches microbiome interactions in cutaneous disorders at the University of Miami Miller School of Medicine and was not involved in the study.

"To identify chronic wound-associated microbiota, Grice’s team swabbed diabetic foot ulcers from 100 participants and sequenced DNA from these samples. Among the bacteria abundantly present in the samples, they identified an environmental, non-pathogenic bacterium called Alcaligenes faecalis. Digging into published datasets, the team found that this bacterium was prevalent in different types of chronic wounds, such as pressure ulcers and venous leg ulcers. This prompted them to investigate the role of A. faecalis in chronic wounds.

***

"Once the cells had formed a layer in the dish, the researchers introduced a thin scratch along the middle, disrupting the continuous layer of cells. They treated the system with either A. faecalis or a control solution and took photographs over time to track how quickly cells from the undisturbed side moved toward the scratch to fill the empty space. Compared to control-treated cells, A. faecalis treatment increased the rate at which keratinocytes migrate. They observed similar results when they repeated this experiment with skin cells obtained from people with diabetes, indicating that the bacterium likely influences wound healing in humans via a similar mechanism.

"To gain insights into how A. faecalis promoted keratinocyte migration, the researchers collected wounds from diabetic mice treated with A. faecalis and sequenced RNA from the tissue. Compared to untreated tissue, wounds treated with A. faecalis exhibited a decrease in expression of several genes. The genes most significantly downregulated encoded matrix metalloproteinases (MMPs), enzymes that break down the extracellular matrix of cells. Previous studies have shown that keratinocytes near the wound edge express MMPs, which helps these cells migrate towards wounds to help them heal.8 However, diabetic conditions promote excessive MMP expression, which is detrimental to wound healing.

"Immunofluorescence analyses of wound tissue from diabetic mice revealed high expression of an MMP near the wound edge, which decreased following A. faecalis­ treatment. Adding MMPs to A. faecalis-treated wounds resulted in these behaving similar to wounds not treated with the bacterium, validating that A. faecalis achieves its pro-healing properties by lowering MMPs at the wound site.

"White was excited by these unexpected findings, adding, “We didn't initially set out to find pro-healing bacteria.” These results offer a new perspective on the wound microbiome. “Most wounds end up healing, which means that not all bacterial colonization is bad. There are also some beneficial bacteria, which we can harness to have wound therapies,” said White.

“'The results show that we need to think about how to retain friendly bacteria while using less aggressive antimicrobial approaches to eliminate pathogens from the chronic wound environment,” said Pastar."

Comment: This research shows that many bacteria are working for the good. This should be remembered when the bad bacteria issue is raised in theodicy discussions.

https://phys.org/news/2024-07-geometry-life-physicists-biofilm-growth.html

"The paper, "The biophysical basis of bacterial colony growth," was published in Nature Physics this week, and it shows that the fitness of a biofilm—its ability to grow, expand, and absorb nutrients from the medium or the substrate—is largely impacted by the contact angle that the biofilm's edge makes with the substrate. The study also found that this geometry has a bigger influence on fitness than anything else, including the rate at which the cells can reproduce.

***

"Understanding how biofilms grow—and what factors contribute to their growth rate—could lead to critical insights on controlling them, with applications for human health, like slowing the spread of infection or creating cleaner surfaces.

***

"While biofilms are ubiquitous in nature, studying them has proven difficult. Because these "cities of microorganisms" are comprised of tiny individuals, scientists have struggled to image them successfully.

***

"Leveraging interferometry, the team began conducting new biofilm experiments, investigating how colonies' shapes changed over time. Co-first author Gabi Steinbach, formerly a postdoctoral scholar in Yunker's lab and now a scientific research coordinator at the University of Maryland, noticed that every colony had a specific shape when it was small: a spherical cap, like a slice from the top of a sphere, or a droplet of water. It's a shape that shows up often in physics, and that sparked the team's interest.

***

"Finally, Thomas Day, a former graduate student in Yunker's lab, now a postdoctoral fellow at the University of Southern California, and one of the authors of the paper, suggested a quirky problem of geometry called the napkin ring problem.

"'As soon as we started to think about the napkin ring problem, we were able to start developing a mathematical toolkit," Yunker says, though the solution wasn't effortless. "We couldn't find anyone who had ever looked at a spherical cap napkin ring before, because the application is very rare."

"Pokhrel, alongside two co-authors, was responsible for working out the geometry. He discovered that the cells grew exponentially at the edge of the shape, expanding further onto the medium, while the cells in the middle grew upward, creating a shape not unlike an egg in a frying pan—if the egg white was expanding outwards, while the yolk was only growing taller.

***

"After incorporating their findings into a mathematical model, the team found that the contact angle was the most important factor: the angle that the very edge of the biofilm made when it touched the surface it was growing on. That single geometric quality is even more important to a biofilm's growth than the rate at which it can reproduce cells.

***

"'Biology is complex," Yunker says. In nature, the surface a biofilm is growing on may not be as consistent as a laboratory surface, and colonies may have different mutations or may consist of more than one species. "But we first needed to understand what happens when temperature and nutrient availability are steady."

"And while the model is based on how biofilms behave in a controlled lab environment, it's a critical first step in understanding how they may behave in nature."

Comment: from 3.5+ billion years ago Australian stromatolites to modern biofilms, bacteria started life and are still here playing an important role in Earth's ecosystems. Usually evolution supplants entire families of organisms. Not bacteria which have a vital role in supporting the structure of life itself. A huge component of allies, with a few bad actors.

https://www.sciencemagazinedigital.org/sciencemagazine/library/item/12_april_2024/41873...

"Coale et al. report a close integration of the endosymbiont into the architecture and function of the host cell, which is a characteristic of organelles. These findings show that UCYN-A has evolved from a symbiont to a eukaryotic organelle for nitrogen fixation—the nitroplast—thereby expanding a function that was thought to be exclusively carried out by prokaryotic cells to eukaryotes.

"Biological nitrogen fixation, which reduces atmospheric dinitrogen gas (N2) into reactive ammonia (NH3), is central in the nitrogen biogeochemical cycle as the only path to incorporate the abundant dinitrogen gas into biomass. This process represents a main driver of fertilization for aquatic and terrestrial systems and is continuously studied to increase crop yields in agriculture. To directly benefit from the resulting ammonia, many photosynthetic organisms, from terrestrial plants to microalgae, incorporate nitrogen-fixing symbionts. This is the case for B. bigelowii and relatives (belonging to the algal class Prymnesiophyceae) that carry the nitrogen-fixing UCYN-A cyanobacteria. The UCYN-A symbiont lacks the genes for the oxygen-evolving photosystem II and carbon fixation, which suggests that it is unable to perform oxygenic photosynthesis and is in-volved in a tight partnership with the host, providing it with fixed nitrogen and receiving fixed carbon in return. This symbiosis is now known to be very stable, to be widespread in sunlit coastal and oceanic waters, and to play a crucial role in the nitrogen biogeochemical cycle. However, challenges in obtaining stable cultures of B. bigelowii and UCYN-A have limited studies on this symbiosis.

***

"The synchronized division and the import of essential eukaryotic proteins indicate that UCYN-A has evolved beyond endosymbiosis (7) and that it can instead be considered a eukaryotic organelle under the full control of the host. The organelle is called the nitroplast, taking the name proposed years ago for analogous systems and denoting its role in nitrogen fixation and its cyanobacterial origin (by analogy to plastids, which are also derived from cyanobacteria).

***

"...the deep cellular integration of UCYN-A into the host and its severe genetic dependency support the view that the nitroplast of B. bigelowii can be added to the short list of endosymbiosis-derived organelles.

***

"The transitions from endosymbionts to the various organelles happened independently at different times of eukaryotic evolution, and this influences their taxonomic coverage. Mitochondria acquisition (thought to have occurred around 2 billion years ago) predates the origin of the eukaryotic cell, and these organelles are found throughout the eukaryotic tree of life, with some cases of secondary loss or modification. The primary endosymbiosis that originated the chloroplast also occurred in ancient times (likely around 1.5 billion years ago) in the supergroup Archaeplastida. Chloroplasts were later transferred to other eukaryotic supergroups by secondary or tertiary endosymbiosis. The establishment of the nitroplast is more recent—about 100 million years ago—and this may explain why this organelle is taxonomically constrained to prymnesiophytes.

***

"The study from Coale et al. shows that a renowned endosymbiont is actually the nitroplast organelle—an optimal adaptation of the microalgae to thrive in nitrogen-limited waters. Like in photosynthesis, a prokaryotic innovation that was incorporated by endosymbiosis into the eukaryotic cell and is now considered a eukaryotic function, these new data support the claim that nitrogen fixation is no longer an exclusive prokaryotic function and that eukaryotes can fix molecular nitrogen through the nitroplast. The nitroplast represents a textbook case of a eukaryotic organelle that complements the energy, carbon, and nitrogen needs of the algal host (see the figure) and is another example of how ecology is the theater where evolution takes place."

Comment: nitrogen is tough to fix, as we know. Here evolution uses a well-worn path to a solution. It is like convergence and can be taken as evidence for design.

https://www.the-scientist.com/an-introduction-to-glycoproteins-71221?utm_campaign=TS_Ne...

"Glycoproteins are a large and diverse group of proteins to which one or more sugar molecules, known as oligosaccharides, have been attached through covalent bonding. These diverse proteins have a wide range of functions, including roles in immune response activation, cell signaling, and disease processes. More than 50 percent of proteins in eukaryotes are known to be glycoproteins, with some predictions being as high as 70 percent.

"The many varieties of glycoproteins differ from each other in several key ways, including the type of oligosaccharide that is attached, its length, whether it is branched or linear, and where on the protein the attachment occurs.

"Glycoproteins are formed through glycosylation, which is a complex and reversible enzymatic reaction that transpires across all domains of life. Glycosylation can occur as a type of post-translational modification (PTM), or it can happen co-translationally, as is the case with N-glycosylation. There are six known types of glycosylation, resulting in different types of glycoproteins, and some glycoproteins bear multiple sites of glycosylation.

***

"The addition of carbohydrates to proteins via glycosylation affects how proteins fold, provides specific instructions on where they will be trafficked, and allows them to perform a wider range of functions.11 Glycoproteins make up the majority of soluble proteins because they are hydrophilic, and most membrane proteins are also glycoproteins. The oligosaccharide chains of membrane glycoproteins are always positioned on the outside of the lipid bilayer of the cell, coating eukaryotic cells with these carbohydrates. This coating is called the cell coat or glycocalyx.

"Glycoproteins are incredibly diverse and have myriad functions within organisms, including roles in development, growth, homeostasis, and survival. They are crucial for cellular interactions; secreted glycoproteins can act as signaling molecules and membrane-bound glycoproteins can function as the surface receptors to which those signaling molecules bind. A key example of this is glycoprotein hormones and their receptors, which are involved in human reproduction.

"Glycoproteins also function extensively in the human innate and adaptive immune system—in fact, almost all immune molecules are glycoproteins. For example, glycoproteins form the T cell receptor complex, the antibodies produced by B cells, and the major histocompatibility complex. Cytokines secreted by immune cells that control inflammation are also glycoproteins.

***

"Glycoproteins also serve important functions in infectious disease, with glycoprotein receptors expressed on viral capsids involved in both recognition and infection of viable host cells. The SARS-CoV-2 virus, which causes COVID-19, gains access to human cells with its spike protein, which is a glycoprotein. Further studies of glycoproteins in humans and microorganisms will expand the understanding of disease pathogenesis and yield a greater range of disease biomarkers and therapeutic targets."

Comment: They are a vital protein molecule which again points to complex design.

https://communities.springernature.com/posts/unlocking-the-secrets-of-nitrogen-fixation...

"Legume plants are unique in their ability to produce specialised root nodules, which host bacteria called rhizobia that convert atmospheric nitrogen into nutrients. Previous research showed that a genetic program for initiating the development of lateral – or secondary – roots also underpins the same process that triggers the formation of these nodules. But the question remained around the additional genetic factors that confer nodule identity as distinct from lateral roots.

"By gene expression profiling and imaging the model legume Medicago truncatula, research carried out as part of the Enabling Nutrient Symbioses in Agriculture (ENSA) project showed that two members of the LIGHT-SENSITIVE SHORT HYPOCOTYL (LSH) family of genes determine the identity of bacterial induced lateral root organs as nodules. This group of factors was previously predominantly known to define the organs and tissues that produce flowers and stems.

"We now understand that LSH1 and LSH2 are instrumental in forming a group of cells that are infectable and habitable by nitrogen-fixing bacteria early during nodule development."

The original paper:

https://www.cell.com/current-biology/fulltext/S0960-9822(24)00018-6?utm_campaign=relate...

"While nodules are unique structures associated with symbiotic bacterial N fixation, we have yet to see any evidence for de novo gene evolution associated with the emergence of nodulation. Rather, we find evidence for the re-networking of preexisting developmental pathways, facilitating the emergence of this novel form of root development. The neo-functionalization of the nodule-specific transcription factor NIN and the associated evolution of cis-regulatory DNA-binding sites in the promoter regions of its downstream targets led to the recruitment of a lateral root organ initiation program into the symbiotic interaction with rhizobial bacteria. Similarly, we hypothesize that further neo-functionalization of NIN provided the opportunity for recruiting a growth-regulatory network with pleiotropic functions in the shoot into the symbiotic root context, thereby promoting the expansion and diversification of the regulatory function of LSH1/LSH2 and their associated downstream regulatory subnetworks into nodule development. This notion is in line with the common principle of morphological evolution as proposed by Carroll,59 in which changes in the spatial and temporal gene expression of preexisting developmental regulators and their associated downstream networks lead to trait divergence and the diversification of novel organ forms and functions. The parallel recruitment of a root initiation program and primordium identity program from the shoot that dictate nodule form and function are essential in non-legume species that are targets for engineering N fixation." (my bold)

Comment: with the largest concentration of gas in the atmosphere, one would think nitrogen is easily obtainable. Unlike oxygen, which is extremely active, nitrogen is really inert. Once again it is specialized bacteria who come to the rescue. Not only does the symbiosis feed each plant, but nitrogen is spread into the soil, reducing the need to spread out fertilizer mixes. How did this evolve? Note my bold. The authors see adaptation of existing parts and processes. But I see it as not that simple. It involves recognizing the need for more nitrogen, then finding the right bacteria to fit into a newly created home, the extremely specialized nodule. Recognizing the need is the easy part. The rest is a very involved development of morphologic alterations which then involves attracting a specific bacterium. I see design, not a chance happening.

https://www.newscientist.com/article/2415409-some-animal-cells-contain-tiny-tornadoes-t...

"The cells that make up all living things contain a fluid called the cytoplasm, which moves around in a process called cytoplasmic streaming. Although this internal movement was first observed more than a century ago, the full pattern and purpose of such fluid flows remain only partially understood.

***

"The team used simulations to calculate the effect these microtubules and motor proteins might have on the cell’s fluid and vice versa, finding that they could closely reproduce the patterns they found when observing the cells using microscopes.

“'The motor is working on the microtubule: it’s carrying cargo and, as a consequence, it’s stirring the fluid,” says Shvartsman. “Now the fluid can influence the buckling of the microtubules, and all of these together can lead to self-organisation of a flow that spans the cell. This is absolutely remarkable.”

"To properly grow and divide, oocytes need to have a stage where they distribute and mix different cellular ingredients together before fixing certain elements in place. These twisters seem to be an essential part of this early mixing stage, says Shvartsman, and they could occur in other animal egg cells that are sufficiently large.

"Human egg cells are about a fifth as large as fruit fly egg cells and are probably too small for this effect to take place, but many insects, fish and amphibians have larger egg cells where these flows may be important, he says.

“'It’s super interesting from the perspective of how life works,” says Robert Cross at the University of Warwick, UK. “The interesting thing is how little, nanoscale autonomous walking machines which are doing this [cargo] transport generate these very large-scale, organised structures inside the cell. That’s the mind-boggling thing.” However, it’s important to note that the rotations are happening much more slowly than a real tornado, he says."

Comment: the cute talk about tornados is beside the point. All animals are mostly water. That means each person is 90% water.

https://www.newscientist.com/article/2408679-life-may-be-less-chaotic-than-we-thought-s...

"Life may not exist at the “edge of chaos” after all. The long-standing belief has been challenged by computer simulations of dozens of processes within cells.

"A hallmark of chaotic systems is that a small disturbance can lead to an outsized effect. The famous butterfly effect offers a classic example, where a flap of an insect’s wings is proposed to cause a storm many kilometres away. Since the late 1980s, researchers have believed that life has evolved to exist right at the edge of this kind of chaos in its search for the middle ground between being adaptable to the environment and remaining stable enough to survive.

“'The idea of the edge of chaos is that cells want to have as much sensitivity as they possibly can, without going into this chaotic regime where the tiniest breeze makes the cell fall apart,” says Jordan Rozum at Binghamton University in New York. “For a long time, people have thought that this edge of chaos phenomenon happens not only at the level of whole cells or organisms, but also if you look at the specific jobs that the cell has to do.”

***

"Rozum and his colleagues set out to test the edge of chaos idea using dozens of models that are rigorously rooted in biological studies.

"They chose 72 experiment-based models representing processes ranging from cell death to gene regulation in the bacterium Escherichia coli. The models came from the Cell Collective database, which collects the work of many independent researchers.

***

"Across the models, their conclusion was the same: life is remarkably good at recovering from perturbations, which wouldn’t be the case if it existed at the edge of chaos.

"Christof Teuscher at Portland State University in Oregon says the new computational method is an exciting tool and the conclusions it led to complicate the discussion of what exactly the edge of chaos is.

"Though models rigorously rooted in laboratory studies haven’t been so extensively studied before, the new study may still include too few of them for generalising its conclusions to all life, he says. There is no question that living organisms exist at “sweet spots” somewhere between order and chaos, but it remains an open question how similar those spots are across all life forms and all of life’s processes, says Teuscher.

"For Rozum, the new study is not the nail in the coffin for the edge of chaos hypothesis, but an incentive to characterise it better. While he and his colleagues showed that many cellular processes themselves are far from the edge of chaos, it could still be true that when they all combine the cell as a whole moves closer to chaos, he says. The researchers plan on studying that idea next, using even more complex computer simulations."

Comment: 'at the edge of chaos' implies the cell might degenerate in functions if a mistake happens. That does not appear to be the case. Cells continue to function with a mistake.

https://www.the-scientist.com/news/a-double-lock-gates-calcium-signaling-71485

Now, an international collaboration led to two papers published in Science Signaling on the mechanisms that open calcium floodgates, revealing a potential route to novel therapies while settling a debate along the way.

Ion channels expressed on organelles act like gatekeepers, controlling the passage of calcium from internal stores into the cytosol. Nicotinic acid adenine dinucleotide phosphate (NAADP) is one of many keys that unlock the gate. First discovered in the late 1980s in sea urchin eggs and later found in mammalian cells, NAADP triggers calcium release from lysosomal stores via ion channel activation, specifically a two-pore channel (TPC).

“NAADP is a very curious second messenger,” said Jonathan Marchant, a cell biologist at Medical College of Wisconsin and coauthor on the papers. Although a potent trigger for calcium release, researchers never discovered a direct binding site, or keyhole, for NAADP on TPC. Then, two papers published in 2021, including one from Marchant’s team, provided a missing link.7,8 The studies revealed the molecular identity of a protein, Jupiter microtubule-associated homolog 2 (JPT2), that facilitates NAADP binding to TPC. If NAADP is the handle of the key, then JPT2 is like the blade that slots into the TPC to open its floodgates.

Adding to the excitement in the field, another paper published later that year identified another blade—the protein like-Sm protein 12 (LSM12)—that linked NAADP to the TPC.

***

“The remarkable thing about this latest paper by Marchant's group is they seem to suggest that you need both JTP2 and LSM12 to bind NAADP and interact with the channel to open it,” said Antony Galione, a pharmacologist at the University of Oxford who was not involved in the study. “One binding protein loaded up with NAADP is not enough, which is quite controlled regulation, really.” Thus, TPC have a double lock system in place to gate NAADP-dependent activities.

Comment: again, an example of IC. All parts must work together from the beginning to create the function.

https://www.the-scientist.com/ts-digest/issue/bacterial-time-capsules-21-5?utm_campaign...

"Diet-derived molecules spur a biological mechanism in the lung barriers of mice that prevents viral lung injury.

"Andreas Wack’s research at the Francis Crick Institute focuses on understanding what influences the severity of viral infections in the lungs. An immunologist by training, Wack studied immune and lung epithelial cells for years before realizing that the lung endothelial cells, which are part of the lung barrier, could be key to an organism’s response to a viral infection.

"Evidence suggested that the aryl hydrocarbon receptor (AHR) is essential for airway epithelia and gut barrier immunity. So, Wack led a team of scientists to investigate the function of AHR in the lung endothelium. In the journal Nature, he and his collaborators described how AHR signaling prevents endothelium damage after an infection and pinpointed the contribution of dietary AHR ligands to this end.

“'Looking at the endothelium in terms of barrier function is not entirely new,” said Wolfgang Kuebler, a lung and cardiovascular physiologist at the Charité University Berlin who was not involved in the research. “But looking at how the endothelium regulates the epithelium and thereby improves barrier function, that is what matters because both cells compose the barrier and work together.”

"Wack’s team used mice that either lacked AHR or did not metabolize its ligands, leading them to build up. After a viral infection, mice lacking the receptor showed signs of lung injury that were prevented in animals with excess AHR ligands.

"By assessing gene expression changes in endothelial cells, the team found that AHR-deficient mice showed disruption of the apelin signaling pathway, which is involved in vessel function regulation. Treating mice with apelin reduced lung damage after infection in wild type but not in AHR-deficient mice, suggesting a role for AHR-apelin signaling in lung protection.

"AHR ligands come from the diet (mainly from cruciferous vegetables) or from the metabolism of gut bacteria, so the team next tested whether adding an AHR ligand to the mouse food would affect AHR activity and disease progression. The enriched diet led to fewer signs of lung damage, which according to Wack, provides an example of how gut-derived molecules can affect barrier integrity in other parts of the body.

“'A lesson for all immunologists is that you want to embed your lung immune response research into a bigger context,” said Wack. “The lung is clearly communicating with other barrier sites and organs, and we need to think about this.'”

Comment: amazing, what you eat affects your lungs' health. Your gut biome plays a role, showing the importance of friendly bacteria. Cruciferous vegetables are: "vegetables of the family Brassicaceae (also called Cruciferae) with many genera, species, and cultivars being raised for food production such as cauliflower, cabbage, kale, garden cress, bok choy, broccoli, Brussels sprouts, mustard plant and similar green leaf vegetables." https://en.wikipedia.org/wiki/Cruciferous_vegetables

https://phys.org/news/2023-11-cell-readwrite-mechanism-uncover-gene.html

"'Whether histone modifications are the epigenetic cause for gene expression has remained a hypothesis because no one had ever seen whether histone modifications self-replicate," explains Takashi Umehara of the RIKEN Center for Biosystems Dynamics Research.

"To explore this question, Umehara and his team focused on a protein known as p300/CBP—an enzyme that can both introduce and bind to acetyl-group modifications (acetylations) on histone proteins. Specifically, the researchers were interested in specific acetylations on the histone H3–H4 complex to which p300/CBP binds. These acetylations are known to activate gene expression in nearby DNA sequences.

"But H3–H4 is just one component of a larger "nucleosome" assembly, which also includes the histone H2B–H2A complex. All of these various histones can carry distinct acetylation patterns, and the causal relationships between their acetylations have not been well understood.

***

"The team found that p300/CBP recognizes and binds to specific acetylation marks on the H3–H4 complex. The enzyme then replicates acetylation marks to unacetylated sites of H3–H4, while also transcribing them from H3–H4 to H2B–H2A within the same nucleosome. Since this newly acetylated H2B–H2A complex is more likely to be stripped from the nucleosome, a model emerges in which it finally instructs which genes to be transcribed by the cellular transcription machinery.

"These results provide an unprecedented glimpse into how p300/CBP inherits acetylation marks to newly divided cells and utilizes those marks epigenetically for gene expression. "I could never have imagined such an elegant yin–yang mechanism for the inheritance and expression of epigenetic information," says Umehara."

Comment: another example of design in evolution. Each step must be coordinated between the necessary molecules. Irreducible complexity again.

https://medicalxpress.com/news/2023-11-immune-molecule-aging-lifespan.html

"Aging is a natural process that affects all living organisms, prompting gradual changes in their behavior and abilities. Past studies have highlighted several physiological factors that can contribute to aging, including the body's immune responses, an imbalance between the production of reactive oxygen (i.e., free radicals) and antioxidants, and sleep disturbances.

***

"Researchers at Washington University in St. Louis recently identified an immune molecule that could play a key role in modulating the process of aging and the duration living organism's lifespan.

***

"Our previous research identified a gene called Slpi as the top-upregulated gene in the meninges of old mice. Slpi is evolutionarily conserved and has an ortholog named IM33 in Drosophila, prompting us to turn to flies to study its role in aging, leveraging their powerful genetics and short lifespan," Wangchao Xu, one of the researchers who carried out the study, told Medical Xpress.

"'Concurrently, inspired by our lab's other findings suggesting that cytokines can shape animal behaviors, I used flies to screen for all immune effectors that can modulate fly behaviors and found that IM33 was a modulator of sleep."

***

"When the team knocked down this gene in the immune cells of fruit flies, they found that this increased the level of reactive oxygen species and altered the composition of microbiota in their gut. This resulted in oxidative stress and in an imbalance in bacterial composition (i.e., dysbiosis), which in turn reduced their lifespan. The researchers found that knocking down this gene also caused sleep disturbances, which have also been associated with aging and a shorter lifespan.

"'This is a proof-of-concept study demonstrating that an evolutionarily conserved immune molecule can serve as a messenger, conveying information between the brain and gut to regulate different levels of aging and control lifespan," Xu said. "This function goes beyond its immune role and further strengthens the contribution of neuroimmune interaction to aging.

***

""\'We suggest that peptidoglycan signaling, a conserved immune pathway, in the neuron could be a potentially novel target to slow down aging," Xu added.

"'The mechanisms through which the brain secreted IM33 shapes the gut immune environment remain mysterious and warrant further investigation. Moreover, testing the role of meningeal Slpi in mice will help determine whether this is a shared mechanism throughout evolution and provide additional supportive evidence for future translational studies.'"

Comment: it is not surprising that inflammation, oxidative stress and change in gut biome induces aging. The good our inhabitant microbiome does for us can have a bad side effect.

https://phys.org/news/2023-11-visualize-osmotic-pressure-tissue.html

"In order to survive, organisms must control the pressure inside them, from the single-cell level to tissues and organs. Measuring these pressures in living cells and tissues in physiological conditions is a challenge.

***

"When molecules dissolved in water are separated into different compartments, water has the tendency to flow from one compartment to another to equilibrate their concentrations, a process known as osmosis. If some molecules cannot cross the membrane that separates them, a pressure imbalance—osmotic pressure—builds up between compartments.

***

"Our cells are constantly moving molecules in and out to prevent the pressure build-up from crushing them. To do so, they use molecular pumps that allow them to keep the pressure in check. This osmotic pressure affects many aspects of cells' lives and even sets their size.

"When cells team up to build our tissues and organs, they, too, face a pressure problem: Our vascular system, or organs such as the pancreas or liver, contain fluid-filled cavities known as lumens that are essential for their function. If cells fail to control osmotic pressure, these lumens may collapse or explode, with potentially catastrophic consequences for the organ.

***

"For this pressure sensor, they introduced a water droplet into an oil droplet that permits water to flow through. When these "double-droplets" were exposed to salt solutions of different concentrations, water flowed in and out of the internal water droplet, changing its volume, until pressures were equilibrated. The researchers showed that the osmotic pressure can be measured by simply checking the droplet size. They then introduced these double-droplets into living cells and tissues using glass microcapillaries to reveal their osmotic pressure.

"'It turns out that cells in animal tissues have the same osmotic pressure as plant cells but, unlike plants, they must balance it constantly with their environment to avoid exploding, since they do not have rigid cell walls," Campàs said.

"With this simple concept, this ingenious method now allows scientists to "see" osmotic pressure in a wide range of settings. "We know that several physical processes affect the working of our bodies," Campàs said. "In particular, osmotic pressure is known to play a fundamental role in the building of organs during embryogenesis, and also in the maintenance of healthy adult organs. With this new technique, we now can study how osmotic pressure impacts all these processes directly in living tissues.'"

Comment: the first cells that existed must have had osmotic pressure controls. Only by d eseign.

https://www.newscientist.com/article/2397442-sperm-caught-breaking-newtons-third-law-of...

"To work out how the cells manage to move despite this apparent obstacle, the researchers analysed the motion of sperm and algal cells’ flagella as they swam. They found that these flagella have an unusual property, dubbed “odd” elasticity, which allows them to wave without losing much energy to the surrounding fluid.

"The researchers quantified the cells’ odd elasticity and arrived at a number called the “odd elastic modulus”. The higher this number, the more a flagellum can wave without the surrounding liquid suppressing its motion. This allows the cell to move forward non-reciprocally.

"Clément Moreau at Kyoto University, who also worked on the study, says calculating the odd elastic modulus for many different micro-swimmers could help scientists classify them and work out whether there are additional features that help them disobey Newton’s third law.

"At present, we don’t know of all the microscopic process that help tiny swimmers defy this law of motion, says Piotr Surówka at the Wrocław University of Science and Technology in Poland. He says being able to calculate the odd elastic modulus and similar numbers could help create a “dictionary” of organisms that are capable of non-reciprocal movement."

Comment: sperm have just so much energy stored. They must reach the egg quickly. The mechanics of how their flagella work, but I'll bet it mimics the bacterial method of sliding straight parts. This is a very purposeful design that cannot be developed by chance steps. Beating Newton's Third law is no mean feat.

https://phys.org/news/2023-10-lysosomes-quick-

"The researchers were able to show for the first time that lysosomes undergo a massive transformation. A signaling lipid acts as a switch between the two states.

***

"Nutrient availability in the body is constantly changing. For example, after a full meal, cells have many more nutrients available than at the end of a long night without any food intake. "It is important for all cells and tissues to be able to respond to the current food intake in such a way that certain basic building blocks are always present inside the cell," explained Professor Volker Haucke,

"These basic building blocks are obtained through catabolism, the process by which ingested nutrients are broken down into small components that the cell uses to make the molecules it needs.

"One of the components responsible for this is the lysosome, a membrane-enclosed sac. At the same time, lysosomes are the central monitoring point that determines whether the food supply in the cell is good or bad. When there is a good supply of nutrients, the mTOR signaling pathway on lysosomes is activated, inducing cell division and growth. When nutrients are scarce, the mTOR complex is switched off to stimulate catabolic programs. As a result, lysosomes combine two opposing tasks: degradation and assembly.

***

"In a complex cascade, this process is controlled by signaling lipid molecules that induce either a starved or a fed state. Using correlative light and electron microscopy, the researchers observed that there are two pools of lysosomes in the cell: Small motile ones, located more at the periphery, act as monitoring stations.

"Meanwhile, larger, more static lysosomes, located closer to the nucleus, are responsible for degradation. What changes is the ratio: In a well-fed state, the small motile lysosomes carrying the active mTOR complex predominate, and there are relatively few static lysosomes. When the cell starves, the small motile lysosomes lose the signaling lipid marker for mTOR and acquire a new signaling lipid, activating the digestive enzymes in the lysosome.

"This response is acute, meaning that the cells are transformed immediately, and initial changes can be observed within minutes. The process from destructive to constructive metabolism is completed in one to two hours," reported Michael Ebner.

"The signaling lipids act as a switch that activates or switches off the mTOR complex, depending on nutrient availability. "Lysosome properties change completely, depending on the signaling lipid," emphasized Volker Haucke. This makes the new findings interesting for therapeutic purposes. After all, during active degradation, lysosomes also remove damaged proteins. And if you can flip the signaling lipid switch artificially, you can also influence the metabolic events in the cell."

Comment: Another example of an irreducibly complex set of on/off controls which can only be developed by design.

"'Most of the skin and gut are replaced very fast, most likely within months," Olaf Bergmann, a principal researcher in the Department of Cell and Molecular Biology at the Karolinska Institute in Stockholm, Sweden, told Live Science in an email. Cells in the liver regenerate at a somewhat slower pace, Bergmann and his colleagues reported June 15 in the journal Cell Systems. For the study, the authors analyzed liver tissue using radiocarbon dating and found that most liver cells are replaced within three years.

"However, cells in other organs and systems are even slower to replicate and lag behind the seven-year cut-off.

"For example, "the human heart renews at a rather low rate, with only 40% of all cardiomyocytes [the cells responsible for the contracting force in the heart] exchanged throughout life," Bergmann said. Skeletal cells, meanwhile, need around 10 years to replicate a skeleton in its entirety, according to the New York Times.

"In the brain, cell renewal can be even more leisurely. Scientists have uncovered evidence showing that some neurons in the hippocampus are renewed, but only at a rate of 1.75% annually, according to a 2013 study in Cell. And some types of neurons within the striatum also regenerate, according to a 2014 study in Cell. But other types of neurons stay with a person for their entire lifetime, Bergmann said. And even the distinct cell populations that can rejuvenate are not replaced entirely, but only partly over a lifetime, he said."

How many cells:

https://www.livescience.com/health/anatomy/how-many-cells-are-in-the-human-body-new-stu...

"According to a new analysis of more than 1,500 papers, the average adult male human has around 36 trillion cells — that's 36 followed by 12 zeros — while adult females have 28 trillion and 10-year-old children have about 17 trillion. To arrive at these estimates, the authors of the new study, which was published Monday (Sept. 18) in the journal PNAS, considered the size and number of 400 types of cells in the body across 60 tissues, including muscle, nerve and immune cells.

***

"'Possibly most critical is our estimate of the total number of human lymphocytes, which are vital for our immune function," he said. "We estimate 2 trillion lymphocytes in the human body which is four times higher than prior estimates and could prove important in lymphocyte-related health and disease, such as HIV or leukemia.'"

Comment: Several trillion cells reproduce every day or so. New mutations, mainly as mistakes occur infrequently. Much rarer mistakes result in cancer. The editing systems keep these mistakes at a very low ratio compared to the rate of cell splitting on a daily basis. This is the answer theodicy articles give to complaints about God's works: it is the only system that works. To enjoy this life we must accept it .

https://phys.org/news/2023-07-mitochondria-stress.html

"...This is referred to as the endosymbiotic theory, according to which that one single-celled organism was the primordial mother of all higher cells, out of which all animals, fungi and plants developed. Over the course of billions of years, the encapsulated bacterium became the cell's powerhouse, the mitochondrion, which supplies it with the cellular energy currency ATP.

"It lost a large part of its genetic material—its DNA—and exchanged smaller DNA segments with the mother cell. However, now as in the past, mitochondria divide independently of the cell and possess some genes of their own.

***

"A certain type of mitochondrial stress is caused by misfolded proteins that are not quickly degraded and accumulate in the mitochondrion. The consequences for both the mitochondrion and the cell are dramatic: Misfolded proteins can, for example, disrupt energy production or lead to the formation of larger amounts of reactive oxygen compounds, which attack the mitochondrial DNA and generate further misfolded proteins. In addition, misfolded proteins can destabilize the mitochondrial membranes, releasing signal substances from the mitochondrion that activate apoptosis, the cell's self-destruction program.

"The mitochondrion responds to the stress by producing more chaperones (folding assistants) to fold the proteins in order to reduce the misfolding, as well as protein shredding units that degrade the misfolded proteins. Until now, how cells trigger this protective mechanism was unknown.

***

"The result is that the mitochondria send two chemical signals to the cell when protein misfolding stress occurs: They release reactive oxygen compounds and block the import of protein precursors, which are produced in the cell and are only folded into their functional shape inside the mitochondrion, causing these precursors to accumulate in the cell. Among other things, the reactive oxygen compounds lead to chemical changes in a protein called DNAJA1. Normally, DNAJA1 supports a specific chaperone (folding assistant) in the cell, which molds the cell's newly formed proteins into the correct shape.

"As a consequence of the chemical change, DNAJA1 now increasingly forces itself on the folding assistant HSP70 as its helper. HSP70 then takes special care of the misfolded protein precursors that accumulate around the mitochondrion because of the blocked protein import. By doing so, HSP70 reduces its interaction with its regular partner HSF1. HSF1 is now released and can migrate into the cell nucleus, where it can trigger the anti-stress mechanism for the mitochondrion.

"As Münch explains, "It was very exciting to discover how the two mitochondrial stress signals are combined into one signal in the cell, which then triggers the cell's response to mitochondrial stress. Moreover, in this complex process, which is essentially driven by tiny local changes in concentration, the stress signaling pathways of the cell and the mitochondrion dovetail very elegantly with each other—like the cogs in a clockwork.'"

Comment: this is more easily explained by God, the designer, solving problems than chance mutations doing it.

https://www.sciencealert.com/the-immortal-jellyfish-can-age-in-reverse-and-possibly-liv...

"The 'immortal jellyfish' is so named because it can, theoretically, live forever. For all we know, some of these tiny, translucent blobs have been drifting along since well before the demise of the dinosaurs, around 66 million years ago.

"That might sound fictitious, but the potential to live for millions of years lies well within the realms of biology – at least for this one curious species.

"When an immortal jellyfish (Turritopsis dohrnii) grows old or damaged, the species can evade death by reverting to a baby polyp stage. It does so by reabsorbing its tentacles and coming to rest as a blob of undifferentiated cells somewhere on the seafloor.

"From here, the young polyp can then bud and produce new adult forms, each smaller than the nail on your pinky when fully grown.

"More importantly, these mature buds are genetically identical to the polyp.

***

"The creature was first described by scientists in 1883, but it wasn't until a century later that experts accidentally discovered its eternal life cycle while keeping it in captivity.

"In the years since, studies have shown that colonies of immortal jellyfish kept in the lab can regress into a polyp stage and begin life again up to 10 times in two years.

"The immortal jelly is the only known species that can rejuvenate itself after sexual reproduction, making it 'biologically immortal'.

"While the species is thought to have originated in the Mediterranean, it is now abundant in every ocean in the world.

"Despite its ubiquity, experts still don't quite understand how the jelly lives for so long. In 2022, genomic research on the genus identified no less than a thousand genes related to aging and DNA repair.

"If scientists can figure out which genes are present or missing in the immortal jellyfish, compared to its relatives, it could reveal the cellular mechanisms behind its everlasting life.

"In 2019, scientists first compared the genetic expression of cells from an immortal jellyfish polyp to a newborn adult 'medusa' with tentacles and a bell.

"They found differences in how some cells functioned, which suggests that specialized cells are somehow being reprogrammed, like resetting a clock back in time.

"This doesn't mean that immortal jellyfish can never die; they can still pass away from injury or starvation. But the possibility of life persists for these creatures like no other."

Comment: In the diversity of life anything is possible.

https://www.sciencedaily.com/releases/2023/07/230713192852.htm

"Scientists have discovered a previously unknown 'housekeeping' process in kidney cells that ejects unwanted content, resulting in cells that rejuvenate themselves and remain functioning and healthy. The self-renewal process, which is fundamentally different from how other bodily tissues are thought to regenerate, helps explain how, barring injury or disease, the kidneys can remain healthy for a lifetime.

***

"Unlike the liver and skin, where cells divide to create new daughter cells and regenerate the organ, cells in the proximal tubules of the kidney are mitotically quiescent -- they do not divide to create new cells. In cases of mild injury or disease, kidney cells do have limited repair capabilities, and stem cells in the kidney can form new kidney cells, but only up to a point, said Dr. Jie Zheng, professor of chemistry and biochemistry in the School of Natural Sciences and Mathematics

***

"Research has shown that gold nanoparticles generally pass unscathed through a structure in the kidney called the glomerulus and then travel into proximal tubules, which make up over 50% of the kidney. Proximal tubular epithelial cells have been shown to internalize the nanoparticles, which eventually escape those cells to be excreted in urine. But just how they escape the cells has been unclear.

***

"'Using the EM, we saw gold nanoparticles encapsulated in lysosomes inside of large vesicles in the lumen, which is the space outside the epithelial cells," Yu said.

"Vesicles are small fluid-filled sacks found both inside and outside of cells that transport various substances.

"'But we also observed the formation of these vesicles containing both nanoparticles and organelles outside of cells, and it was not something we had seen before," Yu said.

"The researchers found proximal tubular cells that had formed outwardly facing bulges in their luminal membranes that contained not only gold nanoparticles but also lysosomes, mitochondria, endoplasmic reticulum and other organelles typically confined to a cell's interior. The extruded contents were then pinched off into a vesicle that floated off into the extracellular space.

"'At that moment, we knew this was an unusual phenomenon," Yu said. "This is a new method for cells to remove cellular contents."

"The extrusion-mediated self-renewal mechanism is fundamentally different from other known regenerative processes -- such as cell division -- and housecleaning tasks like exocytosis. In exocytosis, foreign substances such as nanoparticles are encapsulated in a vesicle inside the cell. Then, the vesicle membrane fuses with the inside of the cell's membrane, which opens to release the contents to the outside.

"'What we discovered is totally different from the previous understanding of how cells eliminate particles. There is no membrane fusion in the extrusion process, which eliminates old content from normal cells and allows the cells to update themselves with fresh contents," Huang said. "It happens whether foreign nanoparticles are present or not. It's an intrinsic, proactive process these cells use to survive longer and function properly.'"

Comment: a new method for automatic cellular garbage disposal to preserve kidney function for life.

https://www.the-scientist.com/news-opinion/an-exercise-induced-liver-enzyme-boosts-meta...

"Plenty of scientific evidence indicates that exercise is good for our health. It benefits our hearts, bones, and muscles, boosts brain health, and may even fight off cancer.1,2,3 Now, a study shows that alongside the muscles and heart, the liver contributes to some of the positive effects of exercise.

"Researchers at Stanford University found that after consistent exercise, the liver produces an enzyme that boosts exercise performance, enhances weight loss, and improves glucose tolerance in mice. Published in Cell Metabolism, the study challenges the conventional muscle-centric view of exercise, revealing that tissues throughout the body respond to breaking a sweat.

***

"A particularly striking finding, said Long, was that in response to exercise, liver cells secreted a family of molecules called carboxylesterase 2 (CES2), which were previously thought to be intracellular proteins. Other studies had revealed that boosting CES2 production inside the liver can increase metabolism in mice.6 However, the team showed that CES2 is also released into the body in response to exercise, and it may influence a number of other organ systems.

"To further understand the role of CES2, the researchers genetically engineered mice to overexpress CES2 in their livers and found that the protein improved overall metabolic health. Mice lost weight and had greater endurance and better glucose tolerance than non-genetically engineered mice. The CES2-overexpressing mice could also run faster and for a longer time than their non-genetically engineered counterparts.

"The researchers next genetically engineered a type of CES2 that mice couldn’t keep inside their livers. Mice that expressed this modified CES2 on top of their regular CES2 still experienced increased benefits from exercise compared to normal mice.

"Lisa Chow, an endocrinologist at the University of Minnesota who was not involved in the study, said that the findings were exciting. “When we think about exercise, we always think about the muscle and the heart or the blood vessels. But that's not the case here,” she said.

"However, Chow said that it’s unclear whether exercise, weight loss, or body composition drove the observed changes in protein secretion. In addition, the study was primarily conducted on male mice. “We need to look at female mice and across species, including humans,” Chow said, also noting that considering how the context of exercise, such as time of day, might affect proteins."

Comment: all early hominins and homos lived hard and exercised hard. It is not difficult to imagine beneficial effects would develop.