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Human brains (and the brains of other vertebrates) are able to process information faster because of myelin, a fatty substance that forms a protective sheath over the axons of our nerve cells and speeds up their impulses. How did our neurons evolve myelin sheaths? Part of the answer—which was unknown until now—almost sounds like science fiction.

Led by scientists from Altos Labs-Cambridge Institute of Science, a team of researchers has uncovered a bit of the gnarly past of how myelin ended up covering vertebrate neurons: a molecular parasite has been messing with our genes. Sequences derived from an ancient virus help regulate a gene that encodes a component of myelin, helping explain why vertebrates have an edge when it comes to their brains .

Prehistoric infection

Myelin is a fatty material produced by oligodendrocyte cells in the central nervous system and Schwann cells in the peripheral nervous system. Its insulating properties allow neurons to zap impulses to one another at faster speeds and greater lengths. Our brains can be complex in part because myelin enables longer, narrower axons, which means more nerves can be stacked together.

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Cellulose is the primary component of the cell walls of plants, making it the most common polymer on Earth. It's responsible for the properties of materials like wood and cotton and is the primary component of dietary fiber, so it's hard to overstate its importance to humanity.

Given its ubiquity and the fact that it's composed of a bunch of sugar molecules linked together, its toughness makes it very difficult to use as a food source. The animals that manage to extract significant calories from cellulose typically do so via specialized digestive tracts that provide a home for symbiotic bacteria—think of the extra stomachs of cows and other ruminants.

Amazingly, humans also play host to bacteria that can break down cellulose—something that wasn't confirmed until 2003 (long after I'd wrapped up my education). Now, a new study indicates that we're host to a mix of cellulose-eating bacteria, some via our primate ancestry, and others through our domestication of herbivores such as cows. But urban living has caused the number of these bacteria to shrink dramatically.

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There are many mysteries in life that we end up shrugging off. Why is urine yellow? It just is, right? Rather than flush that 125-year-old question down the toilet, scientists sought out the answer, discovering a previously unknown microbial enzyme was to blame.

The enzyme that has eluded us for so long is now known as bilirubin reductase. It was identified by researcher and assistant professor Brantley Hall of the University of Maryland, who was part of a team based at the university and the National Institutes of Health.

Bilirubin is an orange pigment released by red blood cells after they die. Gut microbes then use bilirubin reductase to break down bilirubin into colorless urobilinogen, which degrades into yellowish urobilin, giving urine that infamous hue. While urobilin previously had an association with the color of urine, the enzyme that starts the process by producing urobilinogen was unknown until now.

Enlarge / The cranium of an individual with mosaic Turner syndrome from an Iron Age site in Somerset, UK. (credit: K. Anastasiadou et al. 2024)

Turner syndrome is a genetic condition in which a (female) person has only one X chromosome instead of two. Scientists have used a new computational method for precisely measuring sex chromosomes to identify the first prehistoric person with this syndrome dating back some 2,500 years ago, according to a recent paper published in the journal Communications Biology. The team identified four other individuals with sex chromosomes outside the usual XX or XY designations: an early medieval individual with Jacobs syndrome (XYY) and three people from various periods with Klinefelter syndrome (XXY). They also identified an Iron Age infant with Down syndrome .

"It’s hard to see a full picture of how these individuals lived and interacted with their society, as they weren’t found with possessions or in unusual graves, but it can allow some insight into how perceptions of gender identity have evolved over time," said co-author Kakia Anastasiadou , a graduate student at the Francis Crick Institute.

Added co-author Rick Schulting, an archaeologist at the University of Oxford, “The results of this study open up exciting new possibilities for the study of sex in the past, moving beyond binary categories in a way that would be impossible without the advances being made in ancient DNA analysis."

Enlarge / Who doesn't thrill to the sight of a microscopic cross-section of a beetle's rectum? You're welcome. (credit: Kenneth Veland Halberg)

There's rarely time to write about every cool science-y story that comes our way. So this year, we're once again running a special Twelve Days of Christmas series of posts, highlighting one science story that fell through the cracks in 2023, each day from December 25 through January 5. Today: red flour beetles can use their butts to suck water from the air, helping them survive in extremely dry environments. Scientists are honing in on the molecular mechanisms behind this unique ability.

The humble red flour beetle ( Tribolium castaneum ) is a common pantry pest feeding on stored grains, flour, cereals, pasta, biscuits, beans, and nuts. It's a remarkably hardy creature, capable of surviving in harsh arid environments due to its unique ability to extract fluid not just from grains and other food sources, but also from the air. It does this by opening its rectum when the humidity of the atmosphere is relatively high, absorbing moisture through that opening, and converting it into fluid that is then used to hydrate the rest of the body.

Scientists have known about this ability for more than a century, but biologists are finally starting to get to the bottom (ahem) of the underlying molecular mechanisms, according to a March paper published in the Proceedings of the National Academies of Science. This will inform future research on how to interrupt this hydration process to better keep red flour beetle populations in check, since they are highly resistant to pesticides. They can also withstand even higher levels of radiation than the cockroach.

Enlarge / The protein structure of CAS, shown with nucleic acids bound. (credit: Bang Wong, Broad Institute )

CRISPR—Clustered Regularly Interspaced Short Palindromic Repeats—is the microbial world’s answer to adaptive immunity. Bacteria don’t generate antibodies when they are invaded by a pathogen and then hold those antibodies in abeyance in case they encounter that same pathogen again, the way we do. Instead, they incorporate some of the pathogen’s DNA into their own genome and link it to an enzyme that can use it to recognize that pathogenic DNA sequence and cut it to pieces if the pathogen ever turns up again.

The enzyme that does the cutting is called Cas, for CRISPR associated. Although the CRISPR-Cas system evolved as a bacterial defense mechanism, it has been harnessed and adapted by researchers as a powerful tool for genetic manipulation in laboratory studies. It also has demonstrated agricultural uses, and the first CRISPR-based therapy was just approved in the UK to treat sickle-cell disease and transfusion-dependent beta-thalassemia.

Now, researchers have developed a new way to search genomes for CRISPR-Cas-like systems. And they’ve found that we may have a lot of additional tools to work with.

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On an island off the coast of New Zealand, in the shadows of a primeval forest, an eerie sound resonates through the night. It's a deep boom that can sometimes be heard from miles away. This is the mating call of one of the strangest and most intriguing creatures in the region. Meet the critically endangered kākāpō .

Kākāpō (its name means “night parrot” in Māori) are large flightless parrots endemic to New Zealand. In 1894, conservationist Richard Henry relocated mainland birds to a supposedly safe island, but they were met by unsuspected predators. More kākāpō were found on the mainland and some surrounding islands in the 1970s. Though the mainland birds were later moved to those islands, only one survived. He was appropriately named Richard Henry.

The peculiar parrots now roam five islands free of predators, and their population has risen from a precarious 51 in 1995 to 252 in 2022. Still, the limited genetic diversity of such a small population has made breeding problematic. Breeding programs have found that most kākāpō are severely inbred and susceptible to disease and infertility. In an unprecedented move to conserve the species, researchers from the University of Otago have now sequenced the genome of nearly all existing birds in an effort to find out whether there are genetic variants in the population that could help keep the kākāpō from vanishing.

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Multiple lines of evidence indicate that modern humans evolved within the last 200,000 years and spread out of Africa starting about 60,000 years ago. Before that, however, the details get a bit complicated. We're still arguing about which ancestral population might have given rise to our lineage. Somewhere about 600,000 years ago, that lineage split off Neanderthals and Denisovans, and both of those lineages later interbred with modern humans after some of them left Africa.

Figuring out as much as we currently know has required a mix of fossils, ancient DNA, and modern genomes. A new study argues there is another complicating event in humanity's past: a near-extinction period where almost 99 percent of our ancestral lineage died. However, the finding is based on a completely new approach to analyzing modern genomes, and so it may be difficult to validate.

Tracing diversity

Unless a population is small and inbred, they will have genetic diversity: a collection of differences in their DNA ranging from individual bases up to large rearrangements of chromosomes. These differences are tracked when testing services estimate where your ancestors were likely to originate. Some genetic differences arose recently, while others have been floating around our lineage since before modern humans existed.

Enlarge / Study reveals that compared to other contemporary Europeans, Ötzi’s genome had an unusually high proportion of genes in common with those of early farmers from Anatolia. He was also likely bald (or nearly so) when he died. (credit: South Tyrol Museum of Archaeology/Eurac/Marco Samadelli-Gregor Staschitz)

In 1991, a group of hikers found the mummified remains of Ötzi the Iceman emerging from a melting glacier in the Alps—likely murdered, judging by the remains of an arrowhead lodged in his shoulder. The mummy's genome was first sequenced back in 2012, whereby the world learned that he likely had brown eyes, type O blood, blocked arteries, Lyme disease, and lactose intolerance. That first genetic analysis also determined that Ötzi was descended from Steppe Herders hailing from Eastern Europe who migrated to the region some 4,900 years ago.

However, according to a recent paper published in the journal Cell Genomics, Ötzi actually has more common ancestry with early farmers who migrated from Anatolia roughly 8,000 years ago, and the earlier findings were the result of modern DNA contaminating the original sample. The authors also took advantage of the latest advanced sequencing technology to paint a more accurate picture of the Iceman’s appearance and other genetic traits. Most notably, his skin was probably much darker than previously assumed, and he was likely bald, or nearly so, when he died.

As previously reported , archaeologists have spent the last 30 years studying the wealth of information about Copper Age life that Ötzi brought with him into the present. Studies have examined his genome, skeleton, last meals, tattoos, and the microbes that lived in his gut. For instance, in 2016, scientists used DNA sequencing to identify how Ötzi's clothing was made and found that most of it was made from domesticated cattle, goats, and sheep, although his hat was made from brown bear hide and his quiver from a wild roe deer.