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Comment by Dr. Krishna Kumari Challa on September 2, 2021 at 11:37am

Hidden bacterial hairs power nature's 'electric grid'

A hair-like protein hidden inside bacteria serves as a sort of on-off switch for nature's "electric grid," a global web of bacteria-generated nanowires that permeates all oxygen-less soil and deep ocean beds,  researchers report in the journal Nature.

The ground beneath our feet, the entire globe, is electrically wired. These previously hidden bacterial hairs are the molecular switch controlling the release of nanowires that make up nature's electrical grid.

Almost all living things breathe oxygen to get rid of excess electrons when converting nutrients into energy. Without access to oxygen, however, soil bacteria living deep under oceans or buried underground over billions of years have developed a way to respire by "breathing minerals," like snorkeling, through tiny protein filaments called nanowires.

Scientists had thought that the nanowires are made up of a protein called "pili" ("hair" in Latin) that many bacteria show on their surface. This work has reveal that this pili structure is made up of two proteins And instead of serving as nanowires themselves, pili remain hidden inside the bacteria and act like pistons, thrusting the nanowires into the environment. Previously nobody had suspected such a structure.

Just how these soil bacteria use nanowires to exhale electricity, however, has remained a mystery. Now that mystery has been solved.

Understanding how bacteria create nanowires will allow scientists to tailor bacteria to perform a host of functions—from combatting pathogenic infections or biohazard waste to creating living electrical circuits, the authors say. It will also assist scientists seeking to use bacteria to generate electricity, create biofuels, and even develop self-repairing electronics.

Structure of Geobacter pili reveals secretory rather than nanowire behaviour, Nature (2021). DOI: 10.1038/s41586-021-03857-w , www.nature.com/articles/s41586-021-03857-w

https://phys.org/news/2021-09-hidden-bacterial-hairs-power-nature.h...

Comment by Dr. Krishna Kumari Challa on September 2, 2021 at 11:28am

Do genetics control who our friends are? It seems so with mice

Have you ever met someone you instantly liked, or at other times, someone who you knew immediately that you did not want to be friends with, although you did not know why?

Some people speculated that "unconscious" part of the brain enables us to process information spontaneously, when, for example, meeting someone for the first time, interviewing someone for a job, or faced with making a decision quickly under stress.

Now, a new study from the University of Maryland School of Medicine (UMSOM) suggests that there may be a biological basis behind this instantaneous compatibility reaction. A team of researchers showed that variations of an enzyme found in a part of the brain that regulates mood and motivation seems to control which mice want to socially interact with other mice—with the genetically similar mice preferring each other.

These findings may indicate that similar factors could contribute to the social choices people make. Understanding what factors drive these social preferences may help us to better recognize what goes awry in diseases associated with social withdrawal, such as schizophrenia or autism, so that better therapies can be developed.

The study was published on July 28 in Molecular Psychiatry, a Nature publication.

But, let us wait till these results are reproduced several times before coming to a conclusion.

 Abigail J. Smith et al, A genetic basis for friendship? Homophily for membrane-associated PDE11A-cAMP-CREB signaling in CA1 of hippocampus dictates mutual social preference in male and female mice, Molecular Psychiatry (2021). DOI: 10.1038/s41380-021-01237-4

https://medicalxpress.com/news/2021-09-genetics-friends-mice.html?u...

Comment by Dr. Krishna Kumari Challa on September 2, 2021 at 11:20am

Scientists  discover a rare, aggressive form of Alzheimer's that begins in the early 40s

A newly discovered gene mutation linked to early onset Alzheimer's disease has been discovered by an international team of scientists, who traced the DNA flaw through multiple members of a single family.

Alzheimer's has long been known as a mind-robbing disease that that wipes out memories and destroys one's sense of self. Most cases of arise sporadically, emerging after age of 65—transmuting one's golden years into a nightmare marked by an incurable brain disease.

Aside from Alzheimer's dementia that begins sporadically in old age, are insidious familial forms that begin years to decades earlier. Early onset refers Alzheimer's that begins before age 65.

Now, an international team of scientists—led by neurobiologists in Sweden—have identified an extraordinarily rare form of the disease that so far has been found only in one family. This form of Alzheimer's is aggressive, rapid and steals its victims' most productive years along their cognitive functions.

Researchers in Sweden have named this form of Alzheimer's—the Uppsala APP deletion—after the family that's endowed with this notorious DNA miscue. It invariably causes descent into dementia at a young age.

Affected individuals have an age at symptom onset  in their early forties, and suffer from a rapidly progressing disease course.

Researchers found that the mutation accelerates the formation of brain-damaging protein plaques, known as amyloid beta, or more simply as Aβ. The gooey plaques destroy neurons and, as a result, annihilate the executive functions of the brain itself. Neuroscientists basically define executive functions as working memory, mental flexibility and self control.

María Pagnon de la Vega et al, The Uppsala APP deletion causes early onset autosomal dominant Alzheimer's disease by altering APP processing and increasing amyloid β fibril formation, Science Translational Medicine (2021). DOI: 10.1126/scitranslmed.abc6184

https://medicalxpress.com/news/2021-09-scientists-sweden-rare-aggre...

Comment by Dr. Krishna Kumari Challa on September 1, 2021 at 12:33pm

 Winners from the Wellcome Photography Prize 2021: 

Fighting Infections

Comment by Dr. Krishna Kumari Challa on September 1, 2021 at 10:57am

The team was particularly interested in the role of sugar molecules on the spike protein, which are called glycans. To see whether the number, type and position of glycans play a role in the membrane fusion stage of viral cell entry by mediating these intermediate spike formations, they performed thousands of simulations using an all-atom structure-based model. Such models allow prediction of the trajectory of atoms over time, taking into account steric forces—that is, how neighboring atoms affect the movement of others.

The simulations revealed that glycans form a "cage" that traps the "head" of the S2 subunit, causing it to pause in an intermediate form between when it detaches from the S1 subunit and when the viral and cell membranes are fused. When the glycans were not there, the S2 subunit spent much less time in this conformation.

The simulations also suggest that holding the S2 head in a particular position helps the S2 subunit recruit human host cells and fuse with their membranes, by allowing the extension of short proteins called fusion peptides from the virus. Indeed, glycosylation of S2 significantly increased the likelihood that a fusion peptide would extend to the host cell membrane, whereas when glycans were absent, there was only a marginal possibility that this would occur.

 simulations indicate that glycans can induce a pause during the spike protein transition. This provides a critical opportunity for the fusion peptides to capture the host cell.

In the absence of glycans, the viral particle would likely fail to enter the host. Our study reveals how sugars can control infectivity, and it provides a foundation for experimentally investigating factors that influence the dynamics of this pervasive and deadly pathogen.

Esteban Dodero-Rojas et al, Sterically confined rearrangements of SARS-CoV-2 Spike protein control cell invasion, eLife (2021). DOI: 10.7554/eLife.70362

https://phys.org/news/2021-08-sars-cov-dynamics-reveals-opportunity...

part 2 **

Comment by Dr. Krishna Kumari Challa on September 1, 2021 at 10:56am

Model of SARS-CoV-2 dynamics reveals opportunity to prevent COVID-19 transmission

Scientists have simulated the transition of the SARS-CoV-2 spike protein structure from when it recognizes the host cell to when it gains entry, according to a study published today in eLife.

The research shows that a structure enabled by sugar molecules on the spike protein could be essential for cell entry and that disrupting this structure could be a strategy to halt virus transmission.
An essential aspect of SARS-CoV-2's lifecycle is its ability to attach to host cells and transfer its genetic material. It achieves this through its spike protein, which is made up of three separate components—a transmembrane bundle that anchors the spike to the virus, and two S subunits (S1 and S2) on the exterior of the virus. To infect a human cell, the S1 subunit binds to a molecule on the surface of human cells called ACE2, and the S2 subunit detaches and fuses the viral and human cell membranes. Although this process is known, the exact order in which it occurs is as yet undiscovered. Yet, understanding the microsecond-scale and atomic-level movements of these protein structures could reveal potential targets for COVID-19 treatment.
Most of the current SARS-CoV-2 treatments and vaccines have focused on the ACE2 recognition step of virus invasion, but an alternative strategy is to target the structural change that allows the virus to fuse with the human host cell.
But probing these intermediate, transient structures experimentally is extremely difficult, and so researchers now  used a computer simulation sufficiently simplified to investigate this large system but that maintains sufficient physical details to capture the dynamics of the S2 subunit as it transitions between pre-fusion and post-fusion shapes.
part 1

Comment by Dr. Krishna Kumari Challa on September 1, 2021 at 10:35am

Cadherins need calcium ions to complete their connections, so Shim grew the cells with different amounts of calcium and measured their response to electrical stimulation. She saw that the less calcium the cells had, the more fluid they became and the quicker they moved. "It goes really fast.

Calcium has many effects on living tissues, however, so Shim had to confirm that the handshakes were to blame for the slow movement. She grew cells with an antibody that attaches to cadherins. With blocked handshakes, these cells moved more quickly.

After working out the ground rules of cell adhesiveness, the researchers developed a solution to their sticky cell problem. Shim grew a layer of skin cells in a high calcium solution so they made their normal connections. Then she treated the cells with a chemical that grabs up calcium ions to break up the cellular handshakes. When Shim lowered the calcium level and applied the electric field, the cells moved on command. Finally, she restored the high calcium level to reinstate the handshakes, resulting in a healthy and cohesive layer of skin cells.

To demonstrate that this approach has the potential to accelerate healing, Shim performed the above experiment using an electrobioreactor developed in the Cohen lab that mimics the closing of a wound. Unlike other models of electrotaxis where the electric field moves cells in one direction, their new system exposes cells to an electric field focused on the center of the injury. Shim showed that the stimulated tissues successfully came together while the unstimulated ones remained largely separate. Cohen's group described their electrobioreactor in a new paper in Biosensors and Bioelectronics.

part3

Comment by Dr. Krishna Kumari Challa on September 1, 2021 at 10:34am

In their previous work, Cohen's group used electric fields to program thousands of individual cells to move in circles and around corners. Their new study used a model of more mature skin—a single layer of mouse skin cells all latched together—which is harder to control. Instead of moving with the speed and precision of a marching band in response to an electric current, the mature skin cells inched along like a crowd of people holding hands with their neighbors.

The mature skin also posed another problem: Once the leading edge of cells advanced, it would peel away from the petri dish and die. "If you apply a command that differs from what the cells naturally 'want' to do, you get a tug-of-war. The result was the tissues ripped themselves apart.

Cohen and Shim suspected that the "handshakes" between cells prevented the tissue from fluidly following the electrical commands. These handshakes are proteins called cadherins that anchor neighboring cells together. They make tissues cohesive so they can move together but can also create traffic jams when cells don't have space to move.

 Gawoon Shim et al, Overriding native cell coordination enhances external programming of collective cell migration, Proceedings of the National Academy of Sciences (2021). DOI: 10.1073/pnas.2101352118

https://phys.org/news/2021-08-cellular-motion-wound.html?utm_source...

part 2

Comment by Dr. Krishna Kumari Challa on September 1, 2021 at 10:33am

Researchers take step toward using cellular motion to help wound healing

With a technique that overcomes cells' innate social behaviors, researchers have taken an important step in directing skin cells to migrate en masse to close wounds—"literally making skin crawl".

In a new study, the researchers overcame the inertia typical of mature skin tissue by breaking the molecular connections between cells, applying an electrical field to direct their migration and then rebuilding the connections. This novel approach improves the controllability of tissues and may one day help optimize wound healing through electrical stimulation.

Research showed that cells in the body can sense and follow an electric field, a process called electrotaxis. Electric fields generated in the body promote healing by directing cells to move toward the wound and are also vital for growth and development.

Despite promising clinical evidence from decades of use in patients, scientists have yet to work out how cells detect and respond to electric fields or how electrical stimulation can best be applied therapeutically. "It's kind of a black box

 Gawoon Shim et al, Overriding native cell coordination enhances external programming of collective cell migration, Proceedings of the National Academy of Sciences (2021). DOI: 10.1073/pnas.2101352118

part1

Comment by Dr. Krishna Kumari Challa on September 1, 2021 at 10:29am

The right mixture of salts to get life started

In modern organisms, the hereditary material DNA encodes the instructions for the synthesis of proteins—the versatile nanomachines that enable modern cells to function and replicate. But how was this functional linkage between DNA and proteins established? According to the "RNA world" hypothesis, primordial living systems were based on self-replicating RNA molecules. Chemically speaking, RNA is closely related to DNA. However, in addition to storing information, RNA can fold into complex structures that have catalytic activity, similar to the protein nanomachines that catalyze chemical reactions in cells. These properties suggest that RNA molecules should be capable of catalyzing the replication of other RNA strands, and initiating self-sustaining evolutionary processes. Hence, RNA is of particular interest in the context of the origin of life as a promising candidate for the first functional biopolymer.

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New options for sustainable antibiotic therapy

Public health is coming under increasing pressure worldwide due to the antibiotic crisis: the rapid increase in resistance of bacterial pathogens could mean that in the near future bacterial infections that are usually harmless will be difficult or impossible to treat. The spread of antibiotic resistance is based on the ability of pathogens to adapt quickly to the drugs. In principle, evolutionary theory assumes that this adaptation is more difficult when environmental conditions change rapidly. Sequential antibiotic therapy, which involves switching between different antibiotics in a short time, could therefore lead to a reduction in the spread of resistance. This therapeutic approach is usually not considered in medical treatment and is also hardly investigated in basic research—despite the possible long-term benefits.

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