The research suggests that microbes in our ancestors’ intestines split into new evolutionary lineages in parallel with splits in the ape family tree.
This came as a surprise to scientists, who had thought that most of our gut bacteria came from our surroundings – what we eat, where we live, even what kind of medicine we take. The new research suggests that evolutionary history is much more important than previously thought.
“When there were no humans or gorillas, just ancestral African apes, they harboured gut bacteria. Then the apes split into different branches, and there was also a parallel divergence of different gut bacteria,” said Prof Andrew Moeller of the University of California, Berkeley who led the study, published in Science. This happened when gorillas separated somewhere between 10-15 million years ago, and again when humans split from chimps and bonobos 5 million years ago. [Continue reading…]
MIT Technology Review reports: With great power — in this case, a technology that can alter the rules of evolution — comes great responsibility. And since there are “considerable gaps in knowledge” about the possible consequences of releasing this technology, called a gene drive, into natural environments, it is not yet responsible to do so. That’s the major conclusion of a report published today by the National Academies of Science, Engineering, and Medicine.
Gene drives hold immense promise for controlling or eradicating vector-borne diseases like Zika virus and malaria, or in managing agricultural pests or invasive species. But the 200-page report, written by a committee of 16 experts, highlights how ill-equipped we are to assess the environmental and ecological risks of using gene drives. And it provides a glimpse at the challenges they will create for policymakers.
The technology is inspired by natural phenomena through which particular “selfish” genes are passed to offspring at higher rate than is normally allowed by nature in sexually reproducing organisms. There are multiple ways to make gene drives in the lab, but scientists are now using the gene-editing tool known as CRISPR to very rapidly and effectively do the trick. Evidence in mosquitoes, fruit flies, and yeast suggests that this could be used to spread a gene through nearly 100 percent of a population.
The possible ecological effects, intended or not, are far from clear, though. How long will gene drives persist in the environment? What is the chance that an engineered organism could pass the gene drive to an unintended recipient? How might these things affect the whole ecosystem? How much does all this vary depending on the particular organism and ecosystem?
Research on the molecular biology of gene drives has outpaced ecological research on how genes move through populations and between species, the report says, making it impossible to adequately answer these and other thorny questions. Substantially more laboratory research and confined field testing is needed to better grasp the risks. [Continue reading…]
Jim Thomas writes: If there is a prize for the fastest emerging tech controversy of the century the ‘gene drive’ may have just won it. In under eighteen months the sci-fi concept of a ‘mutagenic chain reaction’ that can drive a genetic trait through an entire species (and maybe eradicate that species too) has gone from theory to published proof of principle to massively-shared TED talk (apparently an important step these days) to the subject of a US National Academy of Sciences high profile study – complete with committees, hearings, public inputs and a glossy 216 page report release. Previous technology controversies have taken anywhere from a decade to over a century to reach that level of policy attention. So why were Gene Drives put on the turbo track to science academy report status? One word: leverage.
What a gene drive does is simple: it ensures that a chosen genetic trait will reliably be passed on to the next generation and every generation thereafter. This overcomes normal Mendelian genetics where a trait may be diluted or lost through the generations. The effect is that the engineered trait is driven through an entire population, re-engineering not just single organisms but enforcing the change in every descendant – re-shaping entire species and ecosystems at will.
It’s a perfect case of a very high-leverage technology. Archimedes famously said “Give me a lever long enough and a fulcrum on which to place it, and I shall move the world. ” Gene drive developers are in effect saying “Give me a gene drive and an organism to put it in and I can wipe out species, alter ecosystems and cause large-scale modifications.” Gene drive pioneer Kevin Esvelt calls gene drives “an experiment where if you screw up, it affects the whole world”. [Continue reading…]
Science News reports: Prehumans living around 800,000 years ago in what’s now southeastern Spain were, literally, trailblazers. They lit small, controlled blazes in a cave, a new study finds.
Discoveries in the cave provide the oldest evidence of fire making in Europe and support proposals that members of the human genus, Homo, regularly ignited fires starting at least 1 million years ago, say paleontologist Michael Walker of the University of Murcia in Spain and his colleagues. Fire making started in Africa (SN: 5/5/12, p. 18) and then moved north to the Middle East (SN: 5/1/04, p. 276) and Europe, the researchers conclude in the June Antiquity.
If the age estimate for the Spain find holds up, the new report adds to a “surprising number” of sites from deep in the Stone Age that retain evidence of small, intentionally lit fires, says archaeologist John Gowlett of the University of Liverpool in England.
Excavations conducted since 2011 at the Spanish cave, Cueva Negra del Estrecho del Río Quípar, have uncovered more than 165 stones and stone artifacts that had been heated, as well as about 2,300 animal-bone fragments displaying signs of heating and charring. Microscopic and chemical analyses indicate that these finds had been heated to between 400° and 600° Celsius, consistent with having been burned in a fire. [Continue reading…]
The Cretaceous–Paleogene mass extinction 66m years ago was the most recent of five similar crises to have devastated life on Earth over the last 540m years. It rapidly killed off an estimated 76% of species around the globe, including, most famously, the dinosaurs.
But exactly how this event affected different areas of the globe has not been entirely understood. Some scientists have suggested that creatures living at high latitudes could have been sheltered from the worst effects of the mass extinction. Now our new research, published in the journal Nature Communications, reveals that this wasn’t the case – even marine molluscs in Antarctica were affected.
Scientists are still debating what caused the extinction. Many researchers believe it was a sudden crisis, triggered by a catastrophic asteroid impact. This formed the 200km Chicxulub crater, today buried off Mexico’s Yucatan Peninsula. It also produced a thin layer of rock found all over the world known as the “K–Pg boundary”. This “fallout” layer is rich in debris from the asteroid impact and an element called Iridium, rare on Earth but common in space rocks. It coincides with many of the extinctions in the fossil record to within 32,000 years – a geological blink of an eye.
Emily Singer writes: Early human history was a promiscuous affair. As modern humans began to spread out of Africa roughly 50,000 years ago, they encountered other species that looked remarkably like them — the Neanderthals and Denisovans, two groups of archaic humans that shared an ancestor with us roughly 600,000 years earlier. This motley mix of humans coexisted in Europe for at least 2,500 years, and we now know that they interbred, leaving a lasting legacy in our DNA. The DNA of non-Africans is made up of roughly 1 to 2 percent Neanderthal DNA, and some Asian and Oceanic island populations have as much as 6 percent Denisovan DNA.
Over the last few years, scientists have dug deeper into the Neanderthal and Denisovan sections of our genomes and come to a surprising conclusion. Certain Neanderthal and Denisovan genes seem to have swept through the modern human population — one variant, for example, is present in 70 percent of Europeans — suggesting that these genes brought great advantage to their bearers and spread rapidly.
“In some spots of our genome, we are more Neanderthal than human,” said Joshua Akey, a geneticist at the University of Washington. “It seems pretty clear that at least some of the sequences we inherited from archaic hominins were adaptive, that they helped us survive and reproduce.”
But what, exactly, do these fragments of Neanderthal and Denisovan DNA do? What survival advantage did they confer on our ancestors? Scientists are starting to pick up hints. Some of these genes are tied to our immune system, to our skin and hair, and perhaps to our metabolism and tolerance for cold weather, all of which might have helped emigrating humans survive in new lands.
“What allowed us to survive came from other species,” said Rasmus Nielsen, an evolutionary biologist at the University of California, Berkeley. “It’s not just noise, it’s a very important substantial part of who we are.” [Continue reading…]
Nathaniel Comfort writes: In the Darwinian struggle of scientific ideas, the gene is surely among the select. It has become the foundation of medicine and the basis of vigorous biotechnology and pharmaceutical industries. Media coverage of recent studies touts genes for crime, obesity, intelligence — even the love of bacon. We treat our genes as our identity. Order a home genetic-testing kit from the company 23andMe, and the box arrives proclaiming, “Welcome to you.” Cheerleaders for crispr, the new, revolutionarily simple method of editing genes, foretell designer babies, the end of disease, and perhaps even the transformation of humanity into a new and better species. When we control the gene, its champions promise, we will be the masters of our own destiny.
The gene has now found a fittingly high-profile chronicler in Siddhartha Mukherjee, the oncologist-author of the Pulitzer Prize–winning The Emperor of All Maladies, a history of cancer. The Gene’s dominant traits are historical breadth, clinical compassion, and Mukherjee’s characteristic graceful style. He calls it “an intimate history” because he shares with us his own dawning awareness of heredity and his quest to make meaning of it. The curtain rises on Kolkata, where he has gone to visit Moni, his paternal cousin, who has been diagnosed with schizophrenia. In addition to Moni, two of the author’s uncles were afflicted with “various unravelings of the mind.” Asked for a Bengali term for such inherited illness, Mukherjee’s father replies, “Abheder dosh” — a flaw in identity. Schizophrenia becomes a troubling touchstone throughout the book. But the Indian interludes are tacked onto an otherwise conventional triumphalist account of European-American genetics, written from the winners’ point of view: a history of the emperor of all molecules. [Continue reading…]
Sarah Kaplan writes: Life on Earth used to be simple.
Once upon a time, every organism on the planet was a single, simple cell. Scientists call them prokaryotes. They are about as basic as a living thing can be — just little balloons of DNA and protein, with no grander goals in life than to swim around, eat and occasionally duplicate themselves to produce more swimmers and eaters.
Then, about 1.5 billion years ago, something strange and spectacular happened. One prokaryote engulfed another, and instead of digesting it, he put the little guy to work. They established an endosymbiotic relationship: The smaller internal cell performed lots of helpful tasks — such as making energy and building proteins — and in exchange, the bigger cell kept it safe and well-fed. This lucky bit of teamwork gave rise to the complex (a.k.a. eukaryotic) cell that exists today, from curious single-celled protists to the cells that make up all plants, fungi and animals — including us.
The eukaryotes are a weird and diverse lot, but at the cellular level we’ve all got the same basic components: a nucleus to store our DNA, and mitochondria — the descendants of that ancient swallowed organism — to make energy and perform other essential functions. Other internal structures, called organelles, may vary, but those two are so universal that biologists assumed we couldn’t exist without them.
“They’re part of the definition of eukaryotic cell,” said Anna Karnkowska, an evolutionary biologist at the University of British Columbia. “If you open a biology textbook to a picture of a eukaryotic cell, that’s what you’ll see.”
Which is why she was so shocked to find a eukaryote that didn’t have any mitochondria at all: a single-celled relative of the giardia parasite called Monocercomonoides.
The discovery, which Karnkowska made with other biologists when she was a post-doctoral fellow at Charles University in Prague, seems to rip up that textbook illustration. One of her co-authors compared it to finding a city with no utilities or public works department.
“This is the first example of a eukaryote lacking any form of a mitochondrion,” the researchers write in their study, which was published Thursday in the journal Current Biology, “demonstrating that this organelle is not absolutely essential for the viability of a eukaryotic cell.” [Continue reading…]
Phys.org reports: What is intelligence? The definitions vary, but all infer the use of grey matter, whether in a cat or a human, to learn from experience.
On Wednesday, scientists announced a discovery that turns this basic assumption on its head.
A slime made up of independent, single cells, they found, can “learn” to avoid irritants despite having no central nervous system.
“Tantalizing results suggest that the hallmarks for learning can occur at the level of single cells,” the team wrote in a paper published in the journal Proceedings of the Royal Society B. [Continue reading…]
Ed Yong writes: Evolution works on a strict energy budget. Each adaptation burns through a certain number of calories, and each individual can only acquire so many calories in the course of a day. You can’t have flapping wings and a huge body and venom and fast legs and a big brain. If you want to expand some departments, you need to make cuts in others. That’s why, for example, animals that reproduce faster tend to die earlier. They divert energy towards making new bodies, and away from maintaining their own.
But humans, on the face of it, are exceptional. Compared to other apes, we reproduce more often (or, at least, those of us in traditional societies do) and our babies are bigger when they’re born and we live longer. And, as if to show off, our brains are much larger, and these huge organs sap some 20 percent of our total energy.
“We tend to have our cake and eat it too,” says Herman Pontzer from Hunter College. “These traits that make us human are all energetically costly. And until now, we didn’t really understand how we were fueling them.” [Continue reading…]
Veronique Greenwood writes: The millimeter-long roundworm Caenorhabditis elegans has about 20,000 genes — and so do you. Of course, only the human in this comparison is capable of creating either a circulatory system or a sonnet, a state of affairs that made this genetic equivalence one of the most confusing insights to come out of the Human Genome Project. But there are ways of accounting for some of our complexity beyond the level of genes, and as one new study shows, they may matter far more than people have assumed.
For a long time, one thing seemed fairly solid in biologists’ minds: Each gene in the genome made one protein. The gene’s code was the recipe for one molecule that would go forth into the cell and do the work that needed doing, whether that was generating energy, disposing of waste, or any other necessary task. The idea, which dates to a 1941 paper by two geneticists who later won the Nobel Prize in medicine for their work, even has a pithy name: “one gene, one protein.”
Over the years, biologists realized that the rules weren’t quite that simple. Some genes, it turned out, were being used to make multiple products. In the process of going from gene to protein, the recipe was not always interpreted the same way. Some of the resulting proteins looked a little different from others. And sometimes those changes mattered a great deal. There is one gene, famous in certain biologists’ circles, whose two proteins do completely opposite things. One will force a cell to commit suicide, while the other will stop the process. And in one of the most extreme examples known to science, a single fruit fly gene provides the recipe for more than 38,000 different proteins.
But these are dramatic cases. It was never clear just how common it is for genes to make multiple proteins and how much those differences matter to the daily functioning of the cell. Many researchers have assumed that the proteins made by a given gene probably do not differ greatly in their duties. It’s a reasonable assumption — many small-scale tests of sibling proteins haven’t suggested that they should be wildly different.
It is still an assumption, however, and testing it is quite an endeavor. Researchers would have to take a technically tricky inventory of the proteins in a cell and run numerous tests to see what each one does. In a recent paper in Cell, however, researchers at the Dana-Farber Cancer Institute in Boston and their collaborators reveal the results of just such an effort. They found that in many cases, proteins made by a single gene are no more alike in their behavior than proteins made by completely different genes. Sibling proteins often act like strangers. It’s an insight that opens up an interesting new set of possibilities for thinking about how the cell — and the human body — functions. [Continue reading…]
Ed Yong writes: There are tens of trillions of bacteria in my gut and they are different from those in yours. Why?
This is a really basic question about the human microbiome and, rather vexingly, we still don’t have a good answer. Sure, we know some of the things that influence the roll call of species — diet and antibiotics, to name a few — but their relative importance is unclear and the list is far from complete. That bodes poorly for any attempt to work out whether these microbes are involved in diseases, and whether they can be tweaked to improve our health.
Two new studies have tried to address the problem. They’re the largest microbiome studies thus far published, looking at 1,135 Dutch adults and 1,106 Belgians respectively. Both looked at how hundreds of factors affect the microbiome, including age, height, weight, sleep, medical history, smoking, allergies, blood levels of various molecules, and a long list of foods. Both found dozens of factors that affect either the overall diversity of microbial species, or the abundance of particular ones. And encouragingly, their respective lists overlap considerably.
But here’s the important thing: Collectively, the factors they identified explain a tiny proportion of the variation between people’s microbiomes — 19 percent in the Dutch study, and just 8 percent in the Belgian. Which means we’re still largely in the dark about what makes my microbiome different from yours, let alone whether one is healthier than the other. [Continue reading…]
When we’re born, our lungs are thought to be sterile. But from the moment we take our first breath, our pristine lungs are exposed to all the bugs that are in the air. It has become clear in the last 10 years that the lungs rapidly acquire a population of many different microorganisms (mostly bacteria and viruses) that colonise the lungs and remain with us for the rest of our lives. This population of bugs is called the lung microbiome.
We now know more about the lung microbiome thanks to genetics. In the past, identifying the types of bugs present in the lungs depended on being able to grow them in a laboratory, and for many types of bug this was difficult. The big change that happened recently is our ability to recognise both the different bug species, and their relative abundance, by using DNA sequencing. This can be done either from a sample taken from the lungs or from sputum (the mucus we cough up when we have an infection).
Is the lung microbiome a good or a bad thing?
We all know that bacteria in the lungs can be harmful. When harmful bacteria multiply, they cause pneumonia which, despite the existence of antibiotics, can still be deadly. However, it seems that the lung microbiome usually exists in a balanced state, such that harmful types of bugs do not increase in number sufficiently to cause pneumonia. In fact, it’s possible that the very presence of such a diverse range of bugs in the lungs is one of the reasons it’s quite difficult for harmful bugs to multiply and cause disease.