One gene, LINC00662, sits active in human brain tissue and silent in chimpanzee brain tissue, and the reason is a retrovirus that infected the chimpanzee lineage between 5 million and 7 million years ago and inserted itself next to the gene’s regulatory region, according to a study in Science Advances led by Johan Jakobsson at Lund University, as 404 Media reported. Humans carry no such insertion. That is close to the whole finding, and it is enough to reopen a question that has been open since the virus itself was first catalogued: why two genomes that are overwhelmingly similar produce a human brain that runs roughly three times the volume of a chimpanzee’s.
The retrovirus is PTERV1, Pan troglodytes endogenous retrovirus 1, first described in 2005 when Evan Eichler’s lab scanned the finished chimpanzee genome and found a gammaretrovirus-like sequence present in more than 100 copies per genome — by Science News’ count, as many as 158 — in chimpanzees, gorillas, baboons and macaques, and in none of the genomes of humans, orangutans, siamangs or gibbons, as described in the original PLOS Biology paper. PTERV1’s gag, pol and env genes carry stop codons and kilobase-scale deletions, so the virus can no longer replicate; what moves now is DNA it copied in millions of years ago. A 2011 Genome Research survey of the gorilla genome counted 263 full-length PTERV1 insertions, 99.6% of them at different genomic coordinates than in chimpanzees — evidence the two lineages were infected separately rather than by one virus in a shared ancestor.
The Lund group narrowed that broad picture to one insertion, sitting inside the regulatory region of LINC00662, and dated it to between 1.5 million and 5 million years ago: chimpanzees and bonobos, which split from each other roughly 2 million years ago, share the identical insertion site, while gorillas do not.
How the virus turned off a brain gene
To test what the insertion does, the team grew brain organoids — lab-grown neuron clusters that mimic early fetal brain tissue — from human and chimpanzee stem cells. LINC00662 was active in every human organoid and silent in every chimpanzee one. “The gene was strongly expressed in the human organoids, but not at all in the chimpanzee organoids,” said Patricia Gerdes, the paper’s lead author. The team then deleted the PTERV1 sequence from chimpanzee organoids with CRISPR-Cas9; LINC00662 switched back on. Run the experiment the other way — silence LINC00662 in human organoids — and genes tied to neuronal maturation, outgrowth and synapse formation all drop in expression. “This shows that it is in fact the viral insertion that is responsible for the gene being switched off in chimpanzees,” Gerdes said. In human fetal-brain datasets, LINC00662 activity peaks 10 to 12 weeks after conception, the same window in which cortical neurons are still being generated, then declines toward adulthood.
“The virus we investigated specifically affected chimpanzees. Yet humans and chimpanzees have largely the same genetic makeup,” said Jakobsson, the paper’s senior author. “That is why it is important to understand the differences in how genes are regulated.” Gerdes was more careful about what the organoid result does and doesn’t license: “If humans had the same insertion, it probably would have switched off LINC00662 and altered the development of brain cells,” she said. “But we cannot predict that this would produce a particular brain shape, ability, or behavior. The effect could also depend on the surrounding human DNA and other genes.”
Outside Lund, the caution gets sharper. Ravinder Kanda, a retrovirologist at Oxford Brookes University with no role in the study, told Science News that the team has nailed the molecular mechanism, not its consequences.
They’ve proved that absolutely. How far that goes, I don’t think we can quite say yet.
Kanda also pointed out that PTERV1 is one virus among an unknown number still sitting, unidentified, in primate genomes: “I think there are many, many more retroviruses to be discovered.” Endogenous retroviral sequences of all kinds make up at least 8% of the human and chimpanzee genomes combined, by Science News’ tally — so LINC00662 is one data point in a much larger, still-unmapped archive of ancient infections that may have pushed brain development in either direction.
Faster than a monkey, no neocortex required
The same week’s journals carried a second brain story with its own number. Carrion crows (Corvus corone) tested on a visual-motion task at the University of Tübingen made accurate choices in an average of 235 milliseconds — roughly half the decision time recorded in monkeys or humans on comparable tasks — according to Philipp Schmidbauer and Andreas Nieder, writing in Science. The two crows hit 75% and 73% overall accuracy, rising toward 100% on the easiest trials, with choice-selective neurons in the nidopallium caudolaterale, the avian analog of the primate prefrontal cortex, encoding the eventual decision within about 70 milliseconds of the stimulus appearing. Crow and primate lineages diverged more than 360 million years ago, before either evolved a layered neocortex, so a mammalian cortex is clearly not a precondition for a fast, ramping decision circuit, as covered in more detail here. Nieder’s own explanation for the speed is ecological: flight punishes slow visual processing.
A reused coffin, dated by radiocarbon, not by its inscription
A Roman limestone sarcophagus excavated at Westminster Abbey in 1869 carries a Latin inscription naming its original occupant: Valerius Amandinus, a wealthy Londoner who died sometime between 300 and 400 AD. The bones inside are not his. Warwick Rodwell, the Abbey’s consultant archaeologist, radiocarbon-dated the skeleton to between 987 and 1052 AD, as Live Science reported — roughly six centuries after the coffin was carved. The man was 35 to 49 years old, laid first in a lime-lined timber coffin inside the stone one. Rodwell’s best guess, published in the Journal of the British Archaeological Association, is Ælfwig, Abbot of Westminster from 993 to roughly 1020; his successor Wulnoth, who died in 1049, is the only other candidate whose dates fit. “We have two viable contenders for the occupant of the sarcophagus,” Rodwell wrote. “We do not know the date of birth of either.” Workmen had smashed the sarcophagus open in 1820 and reburied it with the bones jumbled, which is why the identity question took a 2016 conservation reopening, and a decade more of analysis, to get even this far.
A disputed date for a 137-year-old painting
The last number worth checking belongs to a painting, not a genome. Elijah Jeong-hyun Kim’s team at Kyung Hee University argues that the sky in Van Gogh’s The Starry Night matches a specific morning: the pre-dawn sky over Saint-Rémy-de-Provence on July 22, 1889, a month after the painting’s conventional June 1889 dating. The match is measured in degrees, not impressions. The Moon and Venus sat 29.7° apart on July 21 and 18.6° apart on July 22, close to the roughly 18° viewing angle the team reconstructed from a separate Van Gogh landscape sketch of the same hillside, and the canvas’s star pattern tilts at 33.13°, inside the 32.6–35.1° range the team calculated for that morning’s sky, as detailed in Scientific Reports. Donald Olson, an astronomer at Texas State University known for dating paintings by their skies, is not convinced: he told Scientific American that the calculated position of Venus in the new reconstruction doesn’t match the canvas, and that any new date needs to overcome Van Gogh’s own June 18, 1889 letter describing a star study already under way. The angle arithmetic and the artist’s correspondence disagree, and nobody has reconciled them yet.