A human brain gene called BC200 can still jump to new spots in our DNA

A gene that is switched on in human brain cells has turned out to be a jumping gene that never fully gave up jumping. The gene, BC200, descends from a mobile piece of DNA, and researchers led by Cedric Feschotte at Cornell University traced copies of it into a virus that infects human skin. Nothing in the work shows human genomes being reshaped today, but it does show a working gene that kept its old ability to move.

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What a jumping non-coding RNA gene is

BC200 is a non-coding RNA gene, meaning the cell reads it into a short RNA molecule that does its job as RNA and is never translated into a protein. It was first identified in the late 1980s as a highly abundant RNA in human neurons, and it is found only in humans and closely related primates. Evidence suggests it may help regulate how neuronal messenger RNAs are turned into proteins, though its exact role is uncertain.

“Retrotransposition-competent” is the technical way of saying that a gene can still copy and paste itself, a capability the evidence below supports without proving it is active in any particular tissue today. A retrotransposon makes an RNA copy, the RNA is converted back into DNA, and the new DNA is inserted at a different spot in a genome. Most genes that began life as transposons lost that ability long ago and now sit quietly where they landed. BC200 is the exception: it was created from a mobile element, serves a cellular function and, according to the new work, retains its mobility.

The Science study and the poxvirus clue

The study, “Escape of the BC200 gene to a human poxvirus reveals its persistent transposition in primates,” appeared in Science on September 24, 2026, in volume 393, issue 6818, on page 1342. The authors are Pu Gao, Ellen J. Pritham, Feschotte and Cheng Sun. Gao is a graduate student in Sun’s lab at Capital Normal University in Beijing, Pritham was at the University of Texas at Arlington during the work, and Feschotte holds the Barbara McClintock Professorship at Cornell. The paper is listed on the Science website.

The clue came from the virus. The team found BC200-derived sequences inside the molluscum contagiosum virus, a human poxvirus, in what Feschotte told Cornell’s news release was, to his knowledge, the first clear example of a transposon escaping its host genome to hop onto a virus. By ScienceAlert’s account, the researchers screened available poxvirus genomes and found two BC200-derived sequences in this one virus, one covering the gene’s whole Alu-derived domain and a shorter fragment, with nothing similar in the other poxviruses examined.

Feschotte framed the puzzle in plain terms. “Somehow evolution hasn’t been able to untangle these two things,” he said, referring to the gene’s mobile origin and its present-day cellular job, which usually separate once a transposon is put to work.

What was shown and what was not

The care here lies in the evidence. According to ScienceAlert, the team reconstructed the transfer from DNA sequence evidence rather than watching it occur, and the researchers suspect it happened in skin cells because those are the only cells known to be infected by the virus, a proposal rather than a confirmed fact. The same account says BC200 has no transport machinery of its own and likely hitches a ride on LINE-1, another mobile element that supplies the copying enzymes.

The same article reports a human-side signal as well: among 908 people, eight variable BC200-derived insertions were found, two of them widespread across five continental groups, one largely restricted to African individuals and five rarer. Rare insertions point to recent activity, but a copy found in one person does not show it arose in that person’s lifetime. Neither Cornell nor ScienceAlert reports an observation of BC200 jumping inside living human neurons.

BC200 is also present at low levels in sperm and eggs, so in principle it could create inherited insertions, and about half the human genome is transposon-derived. Those are background facts, not findings about present-day genomes. The gene is elevated in the brains of people with Alzheimer’s disease and abnormal in some breast tumors, but those are associations. The authors say mobility could play a role in disease, and the open question the team lists is whether BC200 is actively jumping in any tissue, including cancer cells.

The virus detail carries one more puzzle. Poxvirus genomes have a high deletion rate that should quickly purge sequences the virus does not need, so IFLScience reads the surviving BC200 copies as a sign the virus may be keeping them, an inference that still needs testing. Next, the researchers want to test whether the virus uses BC200 to manipulate infected cells. IFLScience notes the authors are more interested in what the case says about genetic flexibility than in any use against the virus. The findings are covered in the ScienceDaily report of the Cornell release.

This article was produced with the assistance of AI and reviewed by Morning Overview editors prior to publication.

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