evolution in four dimensions...,

evolution-institute |  One of the most mind-expanding books that you’ll ever read is Evolution in Four Dimensions by Eva Jablonka and Marion Lamb. They remind us that evolution is about variation, selection, and heredity, not genes. Genes provide one mechanism of heredity but there are others, including epigenetic mechanisms, forms of social learning found in many species, and forms of symbolic thought that are distinctively human. They provide a concise history of why evolutionary theory became so gene-centric during the 20^th Century and how it needs to be expanded to include the other three dimensions.

Eva Jablonka is a Professor at the Cohn Institute for the History of Philosophy of Science and Ideas at Tel Aviv University in Israel. I talked with her by Skype on November 6 2014. Our conversation provides a panoramic tour of evolutionary theory based on heredity, not just genes.

DSW: Welcome, Eva. I’m so pleased to be talking with you.

EJ: Hello, David.

DSW: I want to talk to you about the definition of evolution and the need for it to go beyond genetic evolution. This is the topic of your great book, Evolution in Four Dimensions, which I have adopted as the first text for almost all of my courses. That’s how much I think of it. Let’s begin by discussing your background. What is your training that enables you to write such a book?

EJ: I am a geneticist. I did a PhD in genetics and molecular biology; in fact, on DNA methylation and chromatin structure. Before that, I did a Masters thesis in microbiology. At the same time, I was deeply interested in philosophy of biology. While I was doing a PhD in genetics, I was also writing papers for philosophy of biology journals. I thought that I should combine the two because theoretical biology and evolutionary biology need a very strong conceptual basis. I ended up being in some kind of twilight zone between the two things. For me it was a productive combination.

DSW: Great! Everyone knows that Darwin knew nothing about genes. For him, evolution was about variation, selection and heredity, a resemblance between parents and offspring. Nevertheless, nowadays, whenever you say the word “evolution,” most people hear “genes.” That’s true for a professional evolutionist, as much as for the lay public. How is it that the study of evolution became gene-centric?

EJ: It is related to the strong focus on heredity that is apparent already in the second 19th century, when many  theories of heredity were developed. Once evolution became an accepted theory it was clear that one has to think very seriously about heredity. In order to have cumulative evolution, heredity is necessary.  Darwin himself had a theory of heredity, which was, in fact, one of the most Lamarckian theories of heredity around at the time!  The point is, however, that he needed a theory of heredity to consolidate his theory of evolution, and he  did develop one.

The other reason heredity became focal was because  of the Industrial Revolution. The population was growing and there was an urgent need to feed people so improvements in agriculture became pertinent. It was clear that breeding and selection were of great importance, and selection must be based on heritable variation. The study of heritable variation was  therefore  important from a practical point of view.

scientists discover LEM

telegraph |  A protein which ‘turbo-charges’ the immune system so that it can fight off any cancer or virus has been discovered by scientists. 

In a breakthrough described as a ‘game-changer’ for cancer treatment, researchers at Imperial College found a previously unknown molecule which boosts the body’s ability to fight off chronic illnesses.

Scientists at Imperial College London, who led the study, are now developing a gene therapy based on the protein and hope to begin human trials in three years.

“This is exciting because we have found a completely different way to use the immune system to fight cancer,” said Professor Philip Ashton-Rickardt, from the Section of Immunobiology in the Department of Medicine at Imperial, who led the study.


“It could be a game-changer for treating a number of different cancers and viruses.

“This is a completely unknown protein. Nobody had ever seen it before or was even aware that it existed. It looks and acts like no other protein.”

The protein – named lymphocyte expansion molecule, or LEM, promotes the spread of cancer killing ‘T cells’ by generating large amounts of energy.

Normally when the immune system detects cancer it goes into overdrive trying to fight the disease, flooding the body with T cells. But it quickly runs out of steam.

inflammatory bowel and ulcerative colitis caused by identified microbe-host interaction

bmj.com |  Objectives Dysbiosis of the intestinal microbiota is associated with Crohn's disease (CD). Functional evidence for a causal role of bacteria in the development of chronic small intestinal inflammation is lacking. Similar to human pathology, TNF^deltaARE mice develop a tumour necrosis factor (TNF)-driven CD-like transmural inflammation with predominant ileal involvement. 

Design Heterozygous TNF^deltaARE mice and wildtype (WT) littermates were housed under conventional (CONV), specific pathogen-free (SPF) and germ-free (GF) conditions. Microbial communities were analysed by high-throughput 16S ribosomal RNA gene sequencing. Metaproteomes were measured using LC-MS. Temporal and spatial resolution of disease development was followed after antibiotic treatment and transfer of microbial communities into GF mice. Granulocyte infiltration and Paneth cell function was assessed by immunofluorescence and gene expression analysis. 

Results GF-TNF^deltaARE mice were free of inflammation in the gut and antibiotic treatment of CONV-TNF^deltaARE mice attenuated ileitis but not colitis, demonstrating that disease severity and location are microbiota-dependent. SPF-TNF^deltaARE mice developed distinct ileitis-phenotypes associated with gradual loss of antimicrobial defence. 16S analysis and metaproteomics revealed specific compositional and functional alterations of bacterial communities in inflamed mice. Transplantation of disease-associated but not healthy microbiota transmitted CD-like ileitis to GF-TNF^deltaARE recipients and triggered loss of lysozyme and cryptdin-2 expression. Monoassociation of GF-TNF^deltaARE mice with the human CD-related Escherichia coli LF82 did not induce ileitis. 

Conclusions We provide clear experimental evidence for the causal role of gut bacterial dysbiosis in the development of chronic ileal inflammation with subsequent failure of Paneth cell function.

Butt then we told you this five years ago....,

viral proteins regulate human embryonic development

phys.org |  A fertilized human egg may seem like the ultimate blank slate. But within days of fertilization, the growing mass of cells activates not only human genes but also viral DNA lingering in the human genome from ancient infections.

Now researchers at the Stanford University School of Medicine have found that the early human cells produce viral proteins, and even become crowded with what appear to be assembled viral particles. These viral proteins could manipulate some of the earliest steps in human development, affecting gene expression and even possibly protecting the cells from further viral infection.

The finding raises questions as to who, or what, is really pulling the strings during human embryogenesis.

"It's both fascinating and a little creepy," said Joanna Wysocka, PhD, associate professor of developmental biology and of chemical and systems biology. "We've discovered that a specific class of viruses that invaded the human genome during recent evolution becomes reactivated in the early development of the human embryo, leading to the presence of viral-like particles and proteins in the human cells."

A paper describing the findings was published online April 20 in Nature. Wysocka is the senior author, and graduate student Edward Grow is the lead author.

Viral particles in the embryo

Retroviruses are a class of virus that insert their DNA into the genome of the host cell for later reactivation. In this stealth mode, the virus bides its time, taking advantage of cellular DNA replication to spread to each of an infected cell's progeny every time the cell divides. HIV is one well-known example of a retrovirus that infects humans.

When a retrovirus infects a germ cell, which makes sperm and eggs, or infects a very early-stage embryo before the germ cells have arisen, the viral DNA is passed along to future generations. Over evolutionary time, however, these viral genomes often become mutated and inactivated. About 8 percent of the human genome is made up of viral sequences left behind during past infections. One retrovirus, HERVK, however, infected humans repeatedly until relatively recently—within about 200,000 years. Much of HERVK's genome is still snuggled, intact, in each of our cells.

Most of these sequences are inactive in mature cells, but recent research has shown that they can spring to life in tumor cells or in human embryonic stem cells. A study published in February in Cell Stem Cell by researchers from Singapore's Genome Institute showed that sequences from a primate virus called HERVH are also activated in early human development.

Now the Stanford researchers have shown for the first time that viral proteins are abundantly present in the developing human embryo and assemble into what appear to be viral particles in electron microscopy images. By following up with additional studies in human embryonic cells grown in vitro, scientists showed that these viral proteins affect gene expression in the developing embryo and may protect the cells from infection by other viruses.

who owns CRISPR?

thescientist |  On April 15, 2014, the US Patent and Trademark Office (USPTO) awarded the first patent for use the CRISPR/Cas system to edit eukaryotic genomes to Feng Zhang of the Broad Institute and MIT. Originally a bacterial or archaeal defense system that uses viral DNA inserted into the genome (CRISPR) as a guide to cut the genomic material of invading viruses with a CRISPR-associated enzyme (Cas), researchers have found many ways to turn the system into a potent and quick way to edit specific genetic sequences. Although there are a handful of other CRISPR-related patents, covering everything from the system’s use in yogurt production to a potential treatment for Huntington’s disease, Zhang’s patent was the first to be granted that covers the technology itself as a platform for a wide array of applications.

However, a patent application filed by Jennifer Doudna of the University of California, Berkeley, and Emmanuelle Charpentier, currently at the Helmholtz Center for Infection Research in Germany, predates Zhang’s by seven months. Zhang’s was most likely granted first because he applied for a fast-track patent, which awarded his intellectual property (IP) six months after he applied. “I think without Zhang fast-tracking his application, the PTO would have flagged it for being in conflict with Doudna’s earlier application,” Jacob Sherkow of the New York Law School wrote in an e-mail to The Scientist. Had his application not been expedited, “we may have been living in a world where there were no issued CRISPR patents” until 2017, he added. The Doudna/Charpentier patent application, assigned to the University of California and the University of Vienna, claims much of the same technology as the Zhang patent, and could be read to cover genome-editing either solely in prokaryotes or in both prokaryotes and eukaryotes. “It’s hard to reconcile 100 percent of both of them,” said Sherkow.

gene-centrism vs. multi-level selection

guardian |  A disagreement between the twin giants of genetic theory, Richard Dawkins and EO Wilson, is now being fought out by rival academic camps in an effort to understand how species evolve.

The learned spat was prompted by the publication of a searingly critical review of Wilson's new book, The Social Conquest of Earth, in Prospect magazine this month. The review, written by Dawkins, author of the popular and influential books The Selfish Gene, The Blind Watchmaker and The God Delusion, has prompted more letters and on-line comment than any other article in the recent history of the magazine and attacks Wilson's theory "as implausible and as unsupported by evidence".

"I am not being funny when I say of Edward Wilson's latest book that there are interesting and informative chapters on human evolution, and on the ways of social insects (which he knows better than any man alive), and it was a good idea to write a book comparing these two pinnacles of social evolution, but unfortunately one is obliged to wade through many pages of erroneous and downright perverse misunderstandings of evolutionary theory," Dawkins writes.

The Oxford evolutionary biologist, 71, has also infuriated many readers by listing other established academics who, he says, are on his side when it comes to accurately representing the mechanism by which species evolve. Wilson, in a short piece penned promptly in response to Dawkins's negative review, was also clearly annoyed by this attempt to outflank him.

"In any case," Wilson writes, "making such lists is futile. If science depended on rhetoric and polls, we would still be burning objects with phlogiston [a mythical fire-like element] and navigating with geocentric maps."

Wilson, 83, is a Harvard professor of evolutionary biology who became famous in the early 1970s with his study of social species in his books The Insect Societiesand Sociobiology. He is internationally acknowledged as "the father of sociobiology" and is the world's leading authority on ants.

For lay spectators, the row is a symptom of the long and controversial evolution of the very idea of evolution. At root it is a dispute about whether natural selection, the theory of "the survival of the fittest" first put forward by Charles Darwin in 1859, occurs only to preserve the single gene. Wilson is an advocate of "multi-level selection theory", a development of the idea of "kin selection", which holds that other biological, social and even environmental priorities may be behind the process.

lucy in the sky with diamonds....,

BI |  John Badding of Penn State University and his team discovered that liquid benzene, when subjected to extreme pressure (around 200,000 times the pressure at the surface of the Earth) and then slowly relieved of that pressure, forms extremely thin, tight rings of carbon that are structurally identical to diamonds.

In other words, if you could unravel a diamond like you can a piece of fabric, you'd get these far-out threads. The result is a chain, thousands of times thinner than a human hair, that has the potential to be the strongest, stiffest material ever discovered. 

The discovery was something of an accident, but far from a hapless one. The team used a large, high-pressure device called the Paris-Edinburgh device at Tennessee's Oak Ridge National Laboratory to compress a 6-millimeter wide quantity of liquid benzene — a huge amount compared with previous experiments. The volume of liquid benzene, coupled with the size of the device, forced them to relieve the pressure more slowly than they would have otherwise.

"It's been known for a long time that if you put benzene under pressure, it’d make a type of polymer," Badding told Business Insider. "An Italian team did a similar experiment and found it was amorphous, disordered, with no pattern to the way material’s held together, kind of like glass. We were trying to make the same material everyone else had made, but in larger quantities."

When they released the pressure, "something interesting happened: the material became ordered," Badding said. The carbon atoms in the liquid benzene arranged themselves so that each was linked with four others, in what's called a tetrahedral structure. Structurally, the threads formed by the liquid benzene are identical to diamond, with each carbon atom linked with four others. You can see what they look like below. 

It was the breakthrough that Badding had been seeking for 20 years.

"Luck favors the prepared mind," Badding said. "I’d love to be able to say I predicted this was going to happen for benzene. I don’t think I can say that. But in a way our studies in benzene were a step in this larger goal, and we just happened to find that faster than we thought we would."

Now that Badding and his colleagues have shown that this structure is possible, the next step is to confirm the precise structure of the material and look for any imperfections that might exist.

"Theory suggests that if you can make the structures perfect, they could be as strong or stronger than carbon nanotubes, but we have not confirmed that experimentally," Badding said.

Going up

Towards the end of his life, science fiction writer Sir Arthur C. Clarke predicted that a space elevator would be built ten years after everybody stopped laughing. By the time he died, in 2008, everybody had.

the body's ecosystem

thescientist |  The human body is teeming with microbes—trillions of them. The commensal bacteria and fungi that live on and inside us outnumber our own cells 10-to-1, and the viruses that teem inside those cells and ours may add another order of magnitude. Genetic analyses of samples from different body regions have revealed the diverse and dynamic communities of microbes that inhabit not just the gut and areas directly exposed to the outside world, but also parts of the body that were long assumed to be microbe-free, such as the placenta, which turns out to harbor bacteria most closely akin to those in the mouth. The mouth microbiome is also suspected of influencing bacterial communities in the lungs. Researchers are also examining the basic biology of the microbiomes of the penis, the vagina, and the skin.

“No tissue in the human body is sterile, including reproductive tissues and, for that matter, the unborn child,” Seth Bordenstein, a biologist at Vanderbilt University, says in an e-mail to The Scientist.

Altogether, the members of the human body’s microbial ecosystem make up anywhere from two to six pounds of a 200-pound adult’s total body weight, according to estimates from the Human Microbiome Project, launched in 2007 by the National Institutes of Health (NIH). The gastrointestinal tract is home to an overwhelming majority of these microbes, and, correspondingly, has attracted the most interest from the research community. But scientists are learning ever more about the microbiomes that inhabit parts of the body outside the gut, and they’re finding that these communities are likely just as important. Strong patterns, along with high diversity and variation across and within individuals, are recurring themes in microbiome research. While surveys of the body’s microbial communities continue, the field is also entering a second stage of inquiry: a quest to understand how the human microbiome promotes health or permits disease.

“None of us in the field—and this is true for the gut, this is true for the skin—none of us can actually tell how our experimental observations really relate to human disease, but we’re getting closer to mechanistic insights,” says immunologist Yasmine Belkaid, chief of mucosal immunology at the National Institute of Allergy and Infectious Disease.

cooperative social networking key to helping microbes spread...,

sciencedaily |  Fresh discoveries about how bacteria co-operate with each other when causing infection could help scientists identify animal diseases that might transmit to people.

Bugs that can co-operate best with each other are most likely to be able to jump to new species, including humans, a new study shows.

Bacteria interact by releasing molecules to help them adapt to their environment -- for example, when killing competing infections in their victim. They co-ordinate these actions by releasing tiny amounts of chemicals as signals.

Bacteria that can co-operate to create an environment in which they can thrive are potentially able to infect lots of different species, including humans. Discovering why some diseases are better equipped to infect more species than others -- and therefore could affect humans -- could be valuable in predicting and managing health threats.

Most new human infections arise from diseases that transmit from animals to humans. Many of these cause serious infections and are difficult to control, such as anthrax and the superbug MRSA.

Research led by the University of Edinburgh used a combination of mathematical models and scientific analysis of genetic code in almost 200 types of bacteria. They found that those bugs that carry lots of genes that help them to co-operate are best equipped to adapt to various environments.

Dr Luke McNally of the University of Edinburgh' School of Biological Sciences, who led the study, said: "Humans have been able to colonise almost all of their planet by collectively modifying the environment to suit themselves. Our study shows bugs try to do the same -- co-operation is important for the spread of bacteria to new species."

behavior and the biome: love and early childhood diarrhea

scientificamerican |  It’s not everyday that love and diarrhea come together in theoretical matrimony. Recently, however, a study by an interdisciplinary team of scientists managed to form this near-perfect union. Oh relax. I’m not about to share the sordid details of a revolting new sexual fetish. (That’s for another post.) The research I’m about to tell you about is actually bigger than that. In fact, it’s a pity that the report appeared without much fanfare last year in Evolution and Human Behavior, because when looked at in the right light, there’s a certain quiet beauty to these data in the way that they subtly illuminate gene-environment interactions.

Before we can hope to understand the curious connection between the hellish expunging of our intestinal contents and the type of person that we’re in turn most likely to marry—or simply to screw—it’s necessary to first step back to look at the wider framework in which the study’s main hypothesis was based. Unless you reject evolutionary psychology out of ignorance or spite (or some combination thereof), it’s noncontroversial to say that, all else equal, it’s biologically more adaptive to sexually reproduce with a healthy than with an unhealthy partner. Needless to say, “biologically adaptive” is rarely isomorphic with “nice and kind”, but kind or not, most of us don’t instinctively gravitate to strangers with a death rattle for a cough or get turned on by the sight of someone with random body parts sloughing off. Beyond such truisms, having children with a chronically ill person makes it not only difficult or impossible for that poor individual to “invest” in your mutual offspring, leaving you to shoulder the “costs” of rearing them on your own, the health of your kids (who, let’s not mince words, are the cooing keepers of your eternal genetic promise) may also be compromised if your partner’s disease is heritable.

While it’s all well and good to aim for a healthy baby-mama or baby-daddy, one hitch is that, in the real world, we can’t always count on a conspicuous cue like emaciation or puddles of pus to tip us off about a prospect’s dubious hardiness. Even if that guy giving you eyes looks fit enough now, who’s to say he won’t be the first to drop when the next scourge rolls in? Our ancestors would have faced similar challenges discerning the relative health of viable members of the opposite sex.

The solution to this adaptive problem was mindlessly ingenious. Among other fixes, our brains became aesthetically predisposed to faces that were the best genetic gambles in a world brimming with deleterious pathogens. When looking at aggregate data, these appealing faces tend to belong to folks who are more disease-resistant across the lifespan. Lucky bastards. Now, how to spot these anti-pathogenic lovers. That’s to say, what’s a “pretty face” exactly, and why do we often disagree on others’ attractiveness? Yes, there’s that old facial symmetry giveaway, but debate rages on about the relationship between this variable trait and perceptions of beauty. If you really want to stack the fitness odds in your offspring’s favour, there seems to be a more reliable marker of a person’s health than mere symmetry: having an extremely sex-typical mug. An already impressive, yet still-mounting, body of evidence reveals that the degree of “masculinity” in a man’s face correlates positively with his lifelong health, while the degree of “femininity” in a woman’s face does the same for hers.

“That’s nice,” you’re probably saying to yourself. “But where does diarrhea come into it?” I thought you’d never ask. The authors of this new study, led by the psychologist Mícheál de Barra of Stockholm University, suspected that our behavioral immune system, which is a hypothetical collection of evolved cognitive biases that spur us on to make adaptive decisions in the domain of disease avoidance, may get a sort of laxative fine-tuning during our early child development.

voices from within: gut microbes and the central nervous system

springer |  Recent advances in research have greatly increased our understanding of the importance of the gut microbiota. Bacterial colonization of the intestine is critical to the normal development of many aspects of physiology such as the immune and endocrine systems. It is emerging that the influence of the gut microbiota also extends to modulation of host neural development. Furthermore, the overall balance in composition of the microbiota, together with the influence of pivotal species that induce specific responses, can modulate adult neural function, peripherally and centrally. Effects of commensal gut bacteria in adult animals include protection from the central effects of infection and inflammation as well as modulation of normal behavioral responses. There is now robust evidence that gut bacteria influence the enteric nervous system, an effect that may contribute to afferent signaling to the brain. The vagus nerve has also emerged as an important means of communicating signals from gut bacteria to the CNS. Further understanding of the mechanisms underlying microbiome–gut–brain communication will provide us with new insight into the symbiotic relationship between gut microbiota and their mammalian hosts and help us identify the potential for microbial-based therapeutic strategies to aid in the treatment of mood disorders.

missing microbes: conspicuously obvious once the man points it out...,

martinblaser |   From Missing Microbes by Martin J. Blaser, MD. Blaser, former chair of medicine at NYU and president of the Infectious Diseases Society of America, is one of a growing number of medical practitioners and researchers who believe that we are experiencing a growing array of "modern plagues," and that the cause of these plagues is rooted in our "disappearing microbiota":

"Within the past few decades, amid all of [our] medical advances, something has gone terribly wrong. In many different ways we appear to be getting sicker. You can see the headlines every day. We are suffering from a mysterious array of what I call 'modern plagues': obesity, childhood diabetes, asthma, hay fever, food allergies, esophageal reflux and cancer, celiac disease, Crohn's disease, ulcerative colitis, autism, eczema. In all likelihood you or someone in your family or someone you know is afflicted. Unlike most lethal plagues of the past that struck relatively fast and hard, these are chronic conditions that diminish and degrade their victims' quality of life for decades. ...

"The autoimmune form of diabetes that begins in childhood and requires insulin injections (juvenile or Type I diabetes) has been doubling in incidence about every twenty years across the industrialized world. In Finland, where record keeping is meticulous, the incidence has risen 550 percent since 1950. ... But the disease itself has not changed; something in us has changed. Type I diabetes is also striking younger children. The average age of diagnosis used to be about nine. Now it is around six, and some children are becoming diabetic when they are three.

"The recent rise in asthma, a chronic inflammation of the airways, is similarly alarming. One in twelve people (about 25 million or 8 percent of the U.S. population) had asthma in 2009, compared with one in fourteen a decade earlier. Ten percent of American children suffer wheezing, breathlessness, chest tightness, and coughing; black children have it worst: one in six has the disease. Their rate increased by 50 percent from 2001 through 2009. But the rise in asthma has not spared any ethnicity: the rates were initially different in various groups, and all have been rising. ... No economic or social class has been spared.

"Food allergies are everywhere. A generation ago, peanut allergies were extremely rare. ... Ten percent of children suffer from hay fever. Eczema, a chronic skin inflammation, affects more than 15 percent of children and 2 percent of adults in the United States. In industrialized nations, the number of kids with eczema has tripled in the past thirty years. ...

"Why are all of these maladies rapidly rising at the same time across the developed world and spilling over into the developing world as it becomes more Westernized? Can it be a mere coincidenc

e? If there are ten of these modern plagues, are there ten separate causes? That seems unlikely.

"Or could there be one underlying cause fueling all these parallel increases? A single cause is easier to grasp; it is simpler, more parsimonious. But what cause could be grand enough to encompass asthma, obesity, esophageal reflux, juvenile diabetes, and allergies to specific foods, among all of the others? Eating too many calories could explain obesity but not asthma; many of the children who suffer from asthma are slim. Air pollution could explain asthma but not food allergies. ...

"The most popular explanation for the rise in childhood illness is the so-called hygiene hypothesis. The idea is that modern plagues are happening because we have made our world too clean. The result is that our children's immune systems have become quiescent and are therefore prone to false alarms and friendly fire. ...

"We need to look closely at the microorganisms that make a living in and on our bodies, massive assemblages of competing and cooperating microbes known collectively as the microbiome. ... Each of us hosts a ... diverse ecology of microbes that has coevolved with our species over millennia. They thrive in the mouth, gut, nasal passages, ear canal, and on the skin. In women, they coat the vagina. The microbes that constitute your microbiome are generally acquired early in life; surprisingly, by the age of three, the populations within children resemble those of adults. Together, they play a critical role in your immunity as well as your ability to combat disease. In short, it is your microbiome that keeps you healthy. And parts of it are disappearing.

"The reasons for this disaster are all around you, including overuse of antibiotics in humans and animals, Cesarean sections, and the widespread use of sanitizers and antiseptics, to name just a few. ...

"The loss of diversity within our microbiome is far more pernicious [than the overuse of antibiotics and resulting antibiotic resistance]. Its loss changes development itself, affecting our metabolism, immunity, and cognition.

"I have called this process the 'disappearing microbiota.' It's a funny term that does not immediately roll off your tongue, but I believe it is correct. For a number of reasons, we are losing our ancient microbes. This quandary is the central theme of this book. The loss of microbial diversity on and within our bodies is exacting a terrible price. I predict it will be worse in the future. Just as the internal combustion engine, the splitting of the atom, and pesticides all have had unanticipated effects, so too does the abuse of antibiotics and other medical or quasi-medical practices (e.g., sanitizer use).

"An even worse scenario is headed our way if we don't change our behavior. It is one so bleak, like a blizzard roaring over a frozen landscape, that I call it 'antibiotic winter.'"

the quantified microbiome visualization looks strangely like an appflow visualization...,

nationalgeographic |  Some of my friends are sporting wristbands these days that keep track of their bodies. Little computers nestled in these device inside record the steps they take each day, the beats of their heart, the length of their slumbers. At the end of each day, they can sit down at a computer and look at their data arrayed across a screen like a seismogram of flesh.

I got one of these devices as a gift recently. But as much as I enjoy wasting time with technology, I just didn’t care enough to put it on my wrist. I already know that I should run more, walk more, stand more, and avoid sitting in front of monitors more. I don’t need granular data to remind me of that.

But as I read the journal Genome Biology today, I decided that someday I might surrender to the Quantified Self movement. I’ll just have to wait till I can track my trillions of microbes from one day to the next.

Thanks to the falling cost of sequencing DNA, it’s now possible for us to survey the thousands of species that live in our bodies. A couple years ago, for example, I found out that I have 58 species in my bellybutton. But all I knew was that there were 58 species in my bellybutton at one point in time–that moment I swiped a Q-tip around my navel. But everything we know about bacteria tells us that our inner ecosystems can change swiftly. My bellybutton may be remarkably different today than it was when I put a Q-tip in it.

Eric Alm, a biologist at MIT, and a graduate student of his named Lawrence David decided to plumb this change by tracking a year in the life of their microbiomes. Each day, they saved some of their stool, and later, they extracted DNA from it to figure out which species of bacteria were living in their guts. David also spat some of his saliva into a tube each day so that he could compare how his microbiome changed in his gut compared to his mouth.

Even though their study only involved two people, it was still very much a Big Data project. And one of the major challenges of any Big Data project is to visualize the results in a useful way. A number on a wrist watch won’t cut it. Between Alm and David, they and their colleagues identified thousands of species of microbes. Most were rare, while a few hundred made up the majority of bugs in their bodies. Some species showed up briefly and vanished; others lingered all year.

Here’s one way to look at their microbiomes. It shows David’s saliva. Each band represents one of the dominant species (or operational taxonomic units). Species belonging to the same lineage (a phylum) have different shades of the same color.  Fist tap Dale.

genetic information transfer promotes cooperation in bacteria

pnas |  Many bacterial species are social, producing costly secreted “public good” molecules that enhance the growth of neighboring cells. The genes coding for these cooperative traits are often propagated via mobile genetic elements and can be virulence factors from a biomedical perspective. Here, we present an experimental framework that links genetic information exchange and the selection of cooperative traits. Using simulations and experiments based on a synthetic bacterial system to control public good secretion and plasmid conjugation, we demonstrate that horizontal gene transfer can favor cooperation. In a well-mixed environment, horizontal transfer brings a direct infectious advantage to any gene, regardless of its cooperation properties. However, in a structured population transfer selects specifically for cooperation by increasing the assortment among cooperative alleles. Conjugation allows cooperative alleles to overcome rarity thresholds and invade bacterial populations structured purely by stochastic dilution effects. Our results provide an explanation for the prevalence of cooperative genes on mobile elements, and suggest a previously unidentified benefit of horizontal gene transfer for bacteria. 

Bacteria often cooperate through the production of public goods that change their environment. These processes can affect human health by increasing virulence or antibiotic resistance. Public good production is costly, making cooperation susceptible to invasion by nonproducing “cheater” individuals. Bacteria also readily share genes, even among distinct species. Our experiments and models converge to show that when both cheating and cooperative genes are transferred, cooperators win against cheaters because transfer increases assortment among alleles, favoring cooperation. This can explain why genes for cooperation are often mobile, and suggests that, in addition to reducing antibiotic resistance spread, preventing gene mobility could reduce cooperative virulence.

bacteria that subsist on electricity

newscientist |   Unlike any other life on Earth, these extraordinary bacteria use energy in its purest form – they eat and breathe electrons – and they are everywhere

STICK an electrode in the ground, pump electrons down it, and they will come: living cells that eat electricity. We have known bacteria to survive on a variety of energy sources, but none as weird as this. Think of Frankenstein's monster, brought to life by galvanic energy, except these "electric bacteria" are very real and are popping up all over the place.

Unlike any other living thing on Earth, electric bacteria use energy in its purest form – naked electricity in the shape of electrons harvested from rocks and metals. We already knew about two types, Shewanella and Geobacter. Now, biologists are showing that they can entice many more out of rocks and marine mud by tempting them with a bit of electrical juice. Experiments growing bacteria on battery electrodes demonstrate that these novel, mind-boggling forms of life are essentially eating and excreting electricity.

That should not come as a complete surprise, says Kenneth Nealson at the University of Southern California, Los Angeles. We know that life, when you boil it right down, is a flow of electrons: "You eat sugars that have excess electrons, and you breathe in oxygen that willingly takes them." Our cells break down the sugars, and the electrons flow through them in a complex set of chemical reactions until they are passed on to electron-hungry oxygen.

In the process, cells make ATP, a molecule that acts as an energy storage unit for almost all living things. Moving electrons around is a key part of making ATP. "Life's very clever," says Nealson. "It figures out how to suck electrons out of everything we eat and keep them under control." In most living things, the body packages the electrons up into molecules that can safely carry them through the cells until they are dumped on to oxygen.

"That's the way we make all our energy and it's the same for every organism on this planet," says Nealson. "Electrons must flow in order for energy to be gained. This is why when someone suffocates another person they are dead within minutes. You have stopped the supply of oxygen, so the electrons can no longer flow."

The discovery of electric bacteria shows that some very basic forms of life can do away with sugary middlemen and handle the energy in its purest form – electrons, harvested from the surface of minerals. "It is truly foreign, you know," says Nealson. "In a sense, alien."

microbial genes, brain & behaviour – epigenetic regulation of the gut–brain axis

wiley |  To date, there is rapidly increasing evidence for host–microbe interaction at virtually all levels of complexity, ranging from direct cell-to-cell communication to extensive systemic signalling, and involving various organs and organ systems, including the central nervous system. As such, the discovery that differential microbial composition is associated with alterations in behaviour and cognition has significantly contributed to establishing the microbiota–gut–brain axis as an extension of the well-accepted gut–brain axis concept. Many efforts have been focused on delineating a role for this axis in health and disease, ranging from stress-related disorders such as depression, anxiety and irritable bowel syndrome to neurodevelopmental disorders such as autism. There is also a growing appreciation of the role of epigenetic mechanisms in shaping brain and behaviour. However, the role of epigenetics in informing host–microbe interactions has received little attention to date. This is despite the fact that there are many plausible routes of interaction between epigenetic mechanisms and the host-microbiota dialogue. From this new perspective we put forward novel, yet testable, hypotheses. Firstly, we suggest that gut-microbial products can affect chromatin plasticity within their host's brain that in turn leads to changes in neuronal transcription and eventually alters host behaviour. Secondly, we argue that the microbiota is an important mediator of gene-environment interactions. Finally, we reason that the microbiota itself may be viewed as an epigenetic entity. In conclusion, the fields of (neuro)epigenetics and microbiology are converging at many levels and more interdisciplinary studies are necessary to unravel the full range of this interaction.

biota, diet, brains, power...,

bbc |  I have some startling news: you are not human. At least, by some counts. While you are indeed made up of billions of human cells working in remarkable concert, these are easily outnumbered by the bacterial cells that live on and in you – your microbiome. There are ten of them for every one of your own cells, and they add an extra two kilograms (4.4lbs) to your body. 

Far from being freeloading passengers, many of these microbes actively help digest food and prevent infection. And now evidence is emerging that these tiny organisms may also have a profound impact on the brain too. They are a living augmentation of your body – and like any enhancement, this means they could, in principle, be upgraded. So, could you hack your microbiome to make yourself healthier, happier, and smarter too?

According to John Cryan, this isn’t as far-fetched as it sounds. As a professor of anatomy and neuroscience at University College Cork, he specialises in the relationship between the brain and the gut. One of his early experiments showed the diversity of bacteria living in the gut was greatly diminished in mice suffering from early life stress. This finding inspired him to investigate the connection between the microbiome and the brain.

The bacterial microbiota in the gut helps normal brain development, says Cryan. “If you don’t have microbiota you have major changes in brain structure and function, and then also in behaviour.” In a pioneering study, a Japanese research team showed that mice raised without any gut bacteria had an exaggerated physical response to stress, releasing more hormone than mice that had a full complement of bacteria. However, this effect could be reduced in bacteria-free mice by repopulating their gut with Bifidobacterium infantis, one of the major symbiotic bacteria found in the gut. Cryan’s team built on this finding, showing that this effect could be reproduced even in healthy mice. “We took healthy mice and fed them Lactobacillus [another common gut bacteria), and we showed that these animals had a reduced stress response and reduced anxiety-related behaviours.” Fist tap Dale.

microbial market theory...,

wustl | The idea that people make calculated decisions that allow them to obtain the most goods with the smallest amount of effort — a complex hypothesis called ‘economic man’ for short — often has been challenged. People sometimes make irrational decisions, they rarely possess sufficient information to make the best decision, and they sometimes act against their own economic self-interest, critics say.

But none of these critiques is as radical as the one advanced in the Jan. 13 online issue of Proceedings of the National Academy of Sciences (PNAS). Written by an international team of researchers, it was inspired by a workshop on biological markets (transactions in which partners, typically animals, exchange commodities for their mutual benefit) held at the Lorentz Center of the University of Leiden in The Netherlands in January. (Visit here for the agenda.)

The scientists asked themselves how far biological market theory, which has been used successfully to explain cooperative behavior in many species, could be extended. Could it be used to describe, for example, the exchange of commodities between organisms without any cognitive ability, such as microbes? 

They could think of instances where single-celled organisms had been shown to avoid bad trading partners, build local business ties, diversify or specialize in a particular commodity, save for a rainy day, eliminate the competition and otherwise behave in ways that seem to follow market-based principles.

They concluded not only that microbes are economic actors, but also that microbial markets can be useful systems for testing questions about biological markets in general, such as the evolution of partner choice, responses to price fluctuations and the identification of market conditions that drive diversification or specialization.

They even foresee practical applications of the work. It might be possible, for example, to manipulate ‘market conditions’ in crop fields to drive nitrogen-fixing bacteria to trade more of their commodity (a biologically available form of nitrogen) with crop plants.

“Creative insights are often easier when theories from one field are explored in a different system as we do here, applying economic concepts to microbial interactions,” said Joan Strassmann, PhD, the Charles Rebstock Professor of Biology in Arts & Sciences at Washington University in St. Louis, who participated in the workshop and helped write the PNAS paper.

“The microscopic nature of microbial systems means it is easy to misunderstand their interactions; an economic framework helps us focus on what is important,” said David Queller, PhD, the Spencer T. Olin Professor of Biology, another of the brainstorming scientists.

from dust-to-dust...,

telegraph | American scientists have made an unsettling discovery. Crop farming across the Prairies since the late 19th Century has caused a collapse of the soil microbia that holds the ecosystem together. 

They do not know exactly what role is played by the bacteria. It is a new research field. Nor do they know where the tipping point lies, or how easily this can be reversed. Nobody yet knows whether this is happening in other parts of the world.

A team at the University of Colorado under Noah Fierer used DNA gene technology to test the 'verrucomicrobia' in Prairie soil, contrasting tilled land with the rare pockets of ancient tallgrass found in cemeteries and reservations. The paper published in the US journal Science found that crop agriculture has "drastically altered" the biology of the land. "The soils currently found throughout the region bear little resemblance to their pre-agricultural state," it concluded.

You might say we already knew this. In fact we did not. There has never before been a metagenomic analysis of this kind and on this scale. Professor Fierer said mankind needs to watch its step. "We really know very little about one of the most productive soils on the planet, but we do know that soil microbes play a key role and we can't just keep adding fertilizers," he said.

The Colorado study has caused a stir in the soil world. It was accompanied by a sobering analysis in Science by academics from South Africa's Witwatersrand University. They fear that we are repeating the mistakes of past civilisations, over-exploiting the land until it goes beyond the point of no return, and leads to a vicious circle of famine, and then social disintegration.

breath straight kicking like cancer....,

thescientist | Fusobacterium nucleatum is a Gram-negative oral commensal microbe, but it has the potential to become pathogenic, occasionally causing periodontal disease. In October 2011, two separate teams from Canada’s BC Cancer Agency and the Broad Institute in Cambridge showed that the bacterium could also be found in the gut, where its abundance was associated with colorectal cancer. Now, two new studies present functional evidence to help explain how F. nucleatum spurs the development of cancer.

In papers published in Cell Host & Microbe today (August 13), teams led by Harvard Medical School’s Aleksandar Kostic and Case Western Reserve University’s Mara Roxana Rubinstein used a mouse model of intestinal tumorigenesis and human colon cancer cells, respectively, to show that F. nucleatum induces proinflammatory and oncogenic activities that promote the growth of colorectal cancer.

“It is usually impossible to infer whether microbes are causative or opportunistic colonizers without functional studies,” said Robert Holt, who led the BC Cancer Agency team that in 2011 reported an association between F. nucleatum in the gut and colorectal cancer but was not involved in the present studies. “Identifying an infectious origin for disease almost always starts with observing an association between the presence of a microbe and the presence of a particular pathology, but an understanding of causality—or lack thereof—requires the gradual accumulation of experimental and epidemiological evidence,” such as that reported today.

The Washington University School of Medicine’s Gautam Dantas agreed that the new work helps distinguish cause from consequence. “Is an observed altered microbiome state in a diseased individual the cause of the disease, or a symptom?” Dantas, who was not involved in the studies, wrote in an e-mail to The Scientist. The papers published today “report on significant strides towards . . . identifying the mechanisms by which a human commensal bacterium, Fusobacterium nucleatum, promotes colorectal cancer.”