AI-generated conceptual illustration of BC200’s transfer from human DNA into a poxvirus, with background neurons representing its association with neuronal regulation.
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Creationists who insist that functional genetic information requires an intelligent designer have another evolutionary history to explain. A genetic element associated with neuronal regulation in primates began as a “jumping gene”, acquired a cellular function, and nevertheless retained its ability to generate copies elsewhere in the genome. Copies even escaped into a human virus. Far from resembling a collection of sealed, immutable designs, genomes reveal a history of copying, repurposing and exchange.
The element is BC200, the subject of a paper in Science by Pu Gao and colleagues, published on 24 September 2026. Its ancestor was a transposable element recruited into a cellular role approximately 40 million years ago. BC200 produces a non-coding RNA: its product is an RNA molecule, rather than a protein. Abundant in neurons, it is thought to help regulate protein production, although its precise physiological role remains incompletely understood.
This is an example of evolutionary exaptation: existing biological material acquires a new use. A sequence whose ancestral significance lay in its capacity to propagate could become useful to its host. No foresight is required. Variants arise without anticipating future needs, and natural selection can preserve those that improve reproductive success. The new function need not have been the reason the original sequence existed.
The unusual feature here is that recruitment did not end BC200’s mobility. Genes derived from transposable elements typically lose that ancestral capacity; BC200 retained it. The researchers identified two independent transfers into molluscum contagiosum virus during the history of modern humans. Whether the acquired sequence benefits the virus remains an open question.
There are two distinct difficulties here for creationism. For young-Earth creationists, the roughly 40-million-year history already places these events far outside their biblical chronology. For intelligent-design advocates, the difficulty is mechanistic: biological function can emerge through the modification and recruitment of material that already exists. Calling the resulting function “designed” adds no explanation of the evidence.
Nor does transfer into a virus mean that a human became a virus, or that every transferred sequence must be adaptive. It demonstrates something more precise: genetic material can cross the boundary between a host genome and a viral genome. BC200’s history combines inherited ancestry, evolutionary repurposing and continuing mobility — exactly the sort of untidy, contingent history that evolutionary biology allows researchers to investigate.
Jumping Genes^ How Genomes Generate Evolutionary Novelty. Genomes are not fixed instruction manuals. They contain sequences that can move or generate copies at new locations, sometimes changing the activity or structure of other genes. These transposable elements, commonly called “jumping genes”, provide one source of the variation on which evolution acts.A Cornell University news release accompanied the paper in Science:
How do genes “jump”?
There are two main routes. Many DNA transposons move by a “cut-and-paste” mechanism: enzymes remove a sequence from one location and insert it elsewhere. Retrotransposons use a “copy-and-paste” mechanism: their DNA is transcribed into RNA, which is then copied back into DNA and inserted at a new location. The original sequence remains, so this process can increase the number of copies.
Some elements encode the machinery needed for their movement; others depend on machinery produced by different mobile elements. “Jumping gene” is therefore a convenient nickname, not a claim that every mobile sequence is a complete, independently functioning gene.
How can this produce new genetic information?
“Genetic information” needs a clear definition. More DNA does not automatically mean more useful biological information. However, transposable elements can produce identifiable, testable changes in what a genome does:
These possibilities have experimental support. For example, research on human immune regulation showed that sequences derived from ancient retroviruses help control certain immune-response genes: deleting particular sequences impaired those genes’ responses. Another study of vertebrate evolution documented repeated recruitment of transposon-derived components into new genes encoding regulators of gene expression.
- New regulatory connections. An inserted element can supply a sequence that helps switch a nearby gene on or off, potentially changing where, when or how strongly it is expressed.
- New components of genes. Parts of mobile elements can become incorporated into gene products. Subsequent evolution can modify these contributions or combine them with existing components.
- New functional genes. Sequences derived from transposable elements can be recruited into cellular roles, producing useful proteins or functional non-coding RNAs.
- Additional material for evolution. Extra copies can accumulate different mutations. Some may eventually acquire functions distinct from those of the ancestral sequence; many others will deteriorate or disappear.
From a mobile element to a cellular function
Recruitment of existing biological material into a new role is called exaptation. BC200 illustrates this process: it originated from a mobile element and became a gene producing a non-coding RNA associated with neuronal regulation. Its unusual feature is that it retained its mobility after acquiring a cellular role.
A sequence can therefore be useful to its host while retaining features inherited from its mobile ancestor. Evolution does not have to erase the old properties before a new function can emerge.
No foresight — and no guarantee of improvement
New insertions can disrupt genes, have little detectable effect, or occasionally prove beneficial. Although insertion sites may be biased towards particular genomic regions, insertions do not occur because an organism anticipates needing a particular improvement.
Natural selection can favour beneficial inherited variants and remove harmful ones, while chance also affects which variants persist. For a new insertion to contribute to evolution across generations, it must enter a lineage of cells that passes DNA to offspring. An insertion confined to an ordinary body cell is generally not inherited.
The important distinction is between generating variation and retaining useful variants. Mobile elements help generate the raw material; mutation, selection and genetic drift shape its subsequent history. There is no requirement for a designer to specify the eventual outcome.
Brief glossary
- Transposon / transposable element
- A DNA sequence capable of moving or generating insertions at new genomic locations. “Transposon” is sometimes used more narrowly for DNA transposons.
- Retrotransposon
- A mobile element that generates new DNA copies through an RNA intermediate.
- Regulatory sequence
- A stretch of DNA that helps control gene activity, including when, where or how strongly a gene is expressed.
- Non-coding RNA
- An RNA molecule that is not translated into a protein. Some non-coding RNAs perform important cellular functions.
- Exaptation
- The recruitment of an existing feature into a new function, including a feature that originally served a different role.
- Genetic drift
- Changes in the frequencies of inherited variants caused by chance sampling between generations.
New type of human jumping gene found in a poxvirus
Scientists found a human genetic element in a poxvirus and discovered it was both an important gene for brain function and a jumping gene capable of moving and inserting itself in genomes.
A study published Sept. 24 in Science reports that the gene, called BC200, combines a mix of characteristics that have never been seen before.
BC200 is mostly expressed in neurons but originated millions of years ago from a transposon or ‘jumping gene’, a non-coding genetic element known for its ability to move and insert itself in genomes.
Transposons can insert blocks of DNA in a gene and disrupt function, leading to disease, but in the long-term they can be a constructive force in evolution to regulate or assemble new beneficial genes. While transposons account for half of human DNA, most of them are inactive, with a very small number of them remaining mobile and able to replicate within genomes.
Until now, no one has observed a human gene that is both mobile and required for bodily functions.
Genes that come from transposable elements and that are repurposed for cellular functions are typically no longer transposable. 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.
Professor Cedric Feschotte, senior author
Barbara McClintock Professor
Department of Molecular Biology and Genetics
College of Agriculture and Life Sciences. Cornell University
Ithaca, NY, USA.
Co-authors include Cheng Sun, professor of evolutionary genomics at Capital Normal University in Beijing, China; and Ellen Pritham, who was an assistant professor at the University of Texas at Arlington when the work was done.
The researchers first identified BC200 in 2010, when Feschotte was a faculty member at University of Texas, Arlington, and Cheng was a postdoctoral researcher in Feschotte’s and Pritham’s joint lab. At the time, Cheng was investigating human transposons in viral genomes using specialized software and genome databases, and he found two insertions of BC200 in a molluscum contagiosum virus (MCV), an infectious but largely benign human poxvirus that causes warts. Though the team recognized the importance of the discovery, they didn’t write a paper on it at the time.
Feschotte and Cheng recently met at a conference, and Cheng mentioned that he and his graduate student, Pu Gao, the paper’s first author, had resurrected the project. “I can’t believe we never got scooped on this,” Feschotte said.
A progenitor of BC200 was co-opted in a common primate ancestor from an ancient transposon roughly 40 million years ago and has jumped to MCV twice within modern human history (since the era of Homo sapiens), about 100,000 years ago.
There have been a few other documented cases of transposable elements in other species inserting in viruses, including in the late 1980s when researchers in a lab setting documented for the first time the insertion of a transposon from moth cells they were studying in culture to a baculovirus, known to infect insects.
This was to my knowledge the first clear example of a transposon escaping its host genome to hop onto a virus, which led to the idea that perhaps if viruses can cross species boundaries, then you may have a mechanism for the spread of these elements across species.
Professor Cedric Feschotte
Then in 2007, a group from Japan discovered a transposable element embedded in a rodent poxvirus, though the transposon originated in a snake, raising the likelihood that the virus also infected reptiles, though it had never been studied.
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.
Professor Cedric Feschotte
BC200 is only found in humans and related primates and was discovered in the late 1980s as an abundant non-coding RNA in human neurons. Although BC200’s physiological function is poorly understood, evidence suggests it may be involved in regulating the translation of neuronal messenger RNAs into proteins. It is also found in low levels in germ cells – sperm and eggs – making it potentially capable of generating inheritable insertions in other areas of the genome.
The researchers also suspect that it jumped in skin cells since these are the only cells known to be infected by MCV. The gene is also aberrantly expressed in some tumors and overexpressed in the brains of Alzheimer’s disease patients, suggesting its jumping ability could also play roles in these diseases.
Feschotte said he and colleagues would like to explore whether the molluscum contagiosum virus is using BC200 for its own purpose of manipulating human host cells. They are also interested in better understanding the gene’s role in disease, such as breast and other types of tumors, where it is abnormally expressed, and whether it is jumping in cancer cells and causing mutations.
Nobel Prize winner Barbara McClintock, Class of 1923, M.A. 1925, Ph.D. 1927, for whom Feschotte’s professorship is named, discovered transposons in the 1940s.
Publication:
BC200 illustrates why evolutionary biology is so productive: it allows researchers to reconstruct how existing genetic material acquired new functions while retaining traces of its ancestry. A mobile element became a functional RNA gene, yet continued to generate insertions and eventually crossed into a viral genome. These are connected stages in an evolutionary history, with no need for a succession of magical creation events.
For creationists who insist that new genetic information requires an intelligent designer, simply pointing to BC200’s function misses the central issue. The question is how that function arose, and its ancestry provides evidence of evolutionary repurposing. An existing sequence can supply material for a new biological role; mutations need not anticipate that role, and natural selection needs no knowledge of the future. Nor must every new copy be useful. Evolution includes unsuccessful variants, neutral changes and occasional innovations that persist.
The remaining uncertainties are equally instructive. Researchers do not yet know whether BC200 benefits the virus, and its precise physiological role in humans still needs further investigation. Science identifies these gaps and turns them into research questions. Declaring that an unspecified designer intended the outcome supplies neither a mechanism nor a testable account of its history.
For young-Earth creationism, there is also the inconvenient matter of roughly 40 million years of primate evolution. For intelligent design, there is the equally inconvenient evidence that genomes acquire functions through copying, modification and recruitment of existing material. BC200 reveals a history shaped by inherited possibilities, chance events and evolutionary processes — without any demonstrated foresight or plan.
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