Asexual organisms typically have gone extinct within one million years because a lack of genetic exchange doesn't allow for the removal of deleterious mutations or the sharing of advantageous ones. But a class of aquatic invertebrates called bdelloid rotifers have persisted for 35 to 40 million years, earning the term "ancient asexuals."
The divergence of alleles into separate genes with different but advantageous functions could explain the puzzling evolutionary success of certain asexual organisms, researchers report today in Science.
"This could point the way, in part, as to why bdelloids are so successful," David Mark Welch of the Marine Biological Laboratory in Woods Hole, Mass., told The Scientist.
Alan Tunnacliffe at the University of Cambridge and his colleagues examined genes associated with surviving dry spells, or desiccation tolerance, and found two copies for lea genes, which are known to preserve enzymes during desiccation in multiple organisms. Their sequences differed by about 13 percent, which is greater than allele differences in sexual animals. The researchers also localized the genes to different chromosomes, which would be expected of alleles from the same gene, and therefore also expected in former alleles.
Tunnacliffe and his colleagues found that the two genes provide different protective benefits to the animal during desiccation. One gene protects proteins from aggregating, while the other appears to associate with the cell membrane, perhaps preventing it from leaking. "Sequence divergence and subsequent functional divergence helped these organisms survive desiccation," Tunnacliffe told The Scientist.
The evidence supports the idea that these were former alleles that accumulated enough mutations to become separate genes, a process termed the "Meselson effect." Matthew Meselson at Harvard University and Mark Welch first described the process in bdelloids in 2000 in a paper that has been cited more than 140 times. The difference in Tunnacliffe's findings, said Mark Welch, is "he was able to come up with some functional assays," rather than just divergent sequences.
Such divergence gives asexual organisms an advantage, the authors argue -- the effect could not occur in sexually reproducing animals, because alleles become homogenized during recombination. The findings suggest asexual reproduction could actually be an "evolutionary mechanism for the generation of diversity," they write.
So far the Meselson effect has not been observed in other organisms, perhaps because the phenomenon is unique and linked to bdelloid's desiccation tolerance, said Mark Welch, who wrote an accompanying commentary in Science. Another reason is that very few asexual organisms do not undergo meiosis, which is part of the definition of the effect.
However, Roger Butlin at the University of Sheffield told The Scientist that additional genes are not necessarily a straightforward solution to asexuality. "Having more copies of genes doesn't get you out of the problem of [disadvantageous] mutation accumulation," he said. "I think we have to look elsewhere for how they've managed to remain asexual for so long." Butlin said bdelloids' large population size and ability to distribute widely might have contributed to their success.
Butlin said the next step will be to look at the evolutionary fates of other gene copies in bdelloids and Tunnacliffe said he will start to look for other functionally divergent genes. "I think this must be going on throughout the genome," Tunnacliffe said.
The authors assume these genes were former alleles, rather than gene duplication, but their assumption makes sense, Mark Welch noted. "If it was a gene duplication, and if we are right about the structure of the bdelloid genome, then there should be four copies," he said. But because Tunnacliffe found only two divergent genes, it appears they were former alleles. "I personally think they've got it right."
Tunnacliffe's functional assays were done in vitro. He said he would like to do more studies on the activities of the two genes' proteins. "What we'd really like to know is, do these proteins do the same job in a living animal?"