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.
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."
"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?"
By Kerry Grens
kgrens@the-scientist.com
Links within this article:
N.N. Pouchkina-Stantcheva et al., "Functional divergence of former alleles in an ancient asexual invertebrate," Science, 318:268-71, 2007.
http://www.sciencemag.org
David Mark Welch
http://jbpc.mbl.edu/labs-markwelch.html
Alan Tunnacliffe
http://www.biot.cam.ac.uk/at/
T. Toma, "Drought resistant gene," The Scientist, March 12, 2002.
http://www.the-scientist.com/article/display/20264/
M. Anderson, "2004 Laskers awarded," The Scientist, September 28, 2004.
http://www.the-scientist.com/article/display/22423/
D. Mark Welch and M. Meselson, "Evidence for the evolution of bdelloid rotifers without sexual recombination or genetic exchange," Science, 288:1211-5, 2000.
http://www.the-scientist.com/10817991
J.B. Weitzman, "Evolving without sex," The Scientist, December 18, 2001.
http://www.the-scientist.com/article/display/20098/
Roger Butlin
http://www.shef.ac.uk/aps/staff/acadstaff/butlin.html
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[Comment posted 2007-10-26 21:13:29]
But, what about divergent species that are spawned from those that have later gone extinct? Is it so important to focus on the species boundaries rather than the continuing population of lineal decendants? What exactly is a species when talking about asexual organisms?
[Comment posted 2007-10-19 12:27:07]
In sharp contradiction to traditional thinking, we have recently introduced a new conceptual framework on why asexual reproduction is linked to high levels of genetic diversity. This is based on our demonstration of the conflict between the gene and genome, and data reinterpretation (Heng, 2007a). In the course of our cancer research we have demonstrated that there are two distinctive phases of somatic evolution. One phase is the punctuated phase where stochastic karyotypic change dominates; the other phase is the stepwise phase where accumulating karyotypes can be clearly traced reflecting system stability (Heng et al, 2006; Heng, 2007b). It is apparent now that the system stability defines the pattern of evolution. By applying this exciting finding to organismal evolution, we quickly realized that the traditional assumption that links sexual reproduction to genetic diversity while linking asexual reproduction to a lack of genetic diversity was incorrect. The reason for such a misunderstanding was due to the confusion over levels of genetic diversity occurring at the gene level or genome level.
In brief, we have found that asexual reproduction is associated with high levels of genetic diversity (both at the genome level and gene level) and the opposite is true for sexual reproduction. Sexual reproduction promotes the continuation of a species by maintaining the chromosome defined boundary or framework of a given system (a species) and that the main purpose of sexual reproduction is the preservation of the identity of a given genome rather than the promotion of genetic diversity as is commonly thought. There is a conflict between the genome level and gene level in terms of genetic diversity. At the genome level during sexual reproduction the key effect is the reduction of genetic diversity enforced by the sexual process and its consequences. At the gene level, however, genetic recombination does generate constrained genetic diversity within the context of the genome. We believe that the genetic diversity occurring at the genome level is much more extensive and significant (Heng, 2007b; Ye et al, 2007). This viewpoint differs fundamentally from conventional models (such as reducing the load of deleterious mutations) as drastic chromosomal aberrations cannot survive the very process of sexual reproduction.
Clearly, the interesting story linking genetic diversity to asexuality supports our new concept, even though it should be pointed out that there will be many diverse genes discovered in asexual species due to the high genome level diversity. In conclusion, the key to the paradox of sex lies at the genome level rather than at the gene level. The time has come for a major conceptual change as confusion over these issues has persisted over 150 years.
References:
1. H.H. Heng, Elimination of altered karyotypes by sexual reproduction preserves species identity. Genome 50: 517-524 (2007)a
2. H.H. Heng et al., Stochastic cancer progression driven by non-clonal chromosome aberrations. J Cell Physiol 208: 461-472 (2006)
3. H.H. Heng, Cancer genome sequencing: the challenge ahead. BioEssays 29: 783-794 (2007)b
4. C.J. Ye et al., The dynamics of cancer chromosome and genome. Cytogenet Genome Res 118:237-246 (2007)
[Comment posted 2007-10-12 11:10:10]
One advantage of sex is to combine favourable mutations into one individual. The world of bdelloid rotifers has not changed much, so rapid evolution is rarely necessary. Individual favourable mutations will be as common as in other species. With a huge population size, two favourable mutations may occur in the same lineage. Small populations won't have two favourable mutations simultaneously anyway, so don't gain from sex either. Bacteria manage quite well being haploid and asexual (although at least some species do transfer DNA).
The other advantage of sex is avoiding accumulation of deleterious mutations. In sexual species some individuals receive many more deleterious alleles than average and their selective death removes many mutant alleles, there is less than one death per deleterious mutation. In asexual species, removal of every deleterious mutation demands death of the lineage containing it, so there is one death (or more) per mutation. Muller?s ratchet clicks around when the lineages with no, or the lowest number of, deleterious mutations become so rare they go extinct. This is an aspect of drift, chance survival. In a very large population, drift is minimal. Bdelloid rotifers must have very large populations, so there may be time for selection to remove individuals carrying deleterious mutations before chance kills off the healthy ones.
Another way to reduce mutational load is to have less genes to mutate. The maximum size of information packages that can be transmitted successfully depends on the error rate, whether we consider the internet or life. The error rate in DNA synthesis evidently requires duplication of information for us diploids with about 20,000 genes to buffer errors which are mostly recessive, but yeast and bacteria with less than 6,000 genes manage nicely as haploids. One might therefore predict that bdelloid rotifers have a relatively low number of genes, say 8,000 to 12,000, as befits a eukaryote behaving like a large microbe. This would be a few thousand more than Plasmodium.
[Comment posted 2007-10-12 05:25:21]
[Comment posted 2007-10-11 20:14:22]