Human neuron gene BC200 left two copies of itself in a wart virus about 100,000 years ago

In 2010, Cheng Sun was a postdoctoral researcher in a joint lab run by Cedric Feschotte and Ellen Pritham at the University of Texas at Arlington ^[7]. He was running specialized software over genome databases to look for human transposons inside viral genomes, and he found two copies of BC200 in molluscum contagiosum virus, a mostly benign human poxvirus that causes warts ^[7]. The team knew the result mattered and did not write a paper at the time. Cheng Sun and his graduate student Pu Gao, now the paper's first author, later revived the project ^[8]. "I can't believe we never got scooped on this," Feschotte said ^[9].

The search design is why the mobility evidence is solid. A human sequence inside a poxvirus genome had to leave its host genome to get there, so the two insertions record BC200 behaving as a jumping gene ^[1]. The researchers date both jumps to about 100,000 years ago, within the era of Homo sapiens ^[11]. The virus is known to infect only skin cells, so they suspect the jumps happened in skin ^[16]. That is a long way from the neurons where BC200 is mostly expressed ^[2].

Transposons make up half of human DNA, but most are inactive and only a very small number can still move ^[3]. The ones put to cellular use usually sit in the inactive group. "Genes that come from transposable elements and that are repurposed for cellular functions are typically no longer transposable," said Feschotte, a senior author of the study ^[5]. His word is "typically," and BC200 is the exception he describes: "BC200 was itself created from a mobile element but has retained its mobility and yet it is also clearly serving a cellular function. Somehow evolution hasn't been able to untangle these two things." ^[6]

The timing adds weight. A BC200 progenitor was co-opted from an ancient transposon into a common primate ancestor roughly 40 million years ago ^[10]. The viral insertions fall in the most recent 0.25 percent of that span ^[12], so the element could still move after nearly its whole history as a co-opted gene.

The evidence on function is thinner. BC200 was discovered in the late 1980s as an abundant noncoding RNA in human neurons, and it exists only in humans and related primates ^[13]. Its physiological function is poorly understood. The evidence suggests it may help regulate the translation of neuronal messenger RNAs into proteins ^[14]. The report's claim of a first human gene both mobile and required for bodily functions ^[4] is therefore much stronger on the first count than the second. The published account does not describe a loss-of-function experiment or a measured rate of new BC200 insertions in human genomes.

Transposons have hopped into viruses before, though rarely on record. In the late 1980s, a lab documented a transposon from cultured moth cells inserting into a baculovirus ^[17]. "This was to my knowledge the first clear example of a transposon escaping its host genome to hop onto a virus," Feschotte said ^[18]. In 2007, a group in Japan found a transposable element of snake origin in a rodent poxvirus ^[19]. "I think at the time it was the first and only case of a clearly vertebrate transposable element escaping into a virus in the wild," Feschotte said ^[20]. BC200 adds a human element to that short list, carried by a poxvirus that infects people ^[7].