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Sex; why even educated fleas do it (02/2006)
One of the great mysteries of biology is why sexual reproduction (SR exists in such a widespread fashion or even why it exists at all. Evolution is the business of keeping the organisms with the characteristics that better fit the environment (have the so called “higher fitness”) and SR does not seem to be an advantageous process. In fact, it not only requires much more energy that asexual reproduction (ASR), but it is also a much less efficient way of producing new individuals and, consequently, of passing on genes to the next generation (as in an ASR population all individuals, and not only females, are able to bear young). Thus, to be maintained as the main form of reproduction, sex must have some crucial unknown evolutionary advantage. And now, in a paper about to be published on the 2nd of March in the journal Nature1, scientists claim to have found new evidence supporting the idea that this evolutionary advantage is an enhanced capacity to eliminate harmful mutations. Purging these mutations leads to “cleaner” genomes, increasing the fitness of the population that use SR, and assuring its preservation throughout evolution.
Sexual reproduction is the process by which two parents, each contributing with half of the offspring DNA, originate a new individual. Additionally, in SR, during the formation of the parental sex cells (egg and sperm) DNA can break and rejoin leading to new arrangements of genes in a process called recombination. This means that the new individual receives a unique mixture of genes from the two parents. When new mutations appear in a SR population this is also the way they are spread, mixed and re-mixed among new individuals.
Scientists have long believed that SR evolutionary advantage resided in this capacity to introduce new variability as an additional source of material for natural selection. But this can only be an improvement if the resulting variability is advantageous, and it is well known that beneficial mutations are extremely rare. So how can SR confer an evolutionary advantage large enough to compensate for its energetic and reproductive disadvantages when compared with ASR?
Several theories have been proposed but, because of the time scale necessary for evolution to occur, their testing has proven difficult. One such theory is the mutational deterministic hypothesis (MDH). MDH proposes that SR advantage resides in its capacity to efficiently eliminate harmful mutations after they are brought together by recombination in one individual. This theory is appealing because, to be true, it requires only two conditions:
That the sexual reproducing population acquire large numbers of harmful mutations every generation – this is relatively easy to be tested, and has been found to be the case in some species, including humans and several viruse
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- That when two harmful mutations come together in a new individual, their effect will be more damaging than the combination of the individual effects of each mutation. This increase in the damaging effect of a mutation, when other harmful mutations are simultaneously present in a genome, is called negative epistasis
The second condition has been more difficult to test, and although negative epistasis is known to occur in nature it is not clear how widespread it is.
But now a Portuguese scientist Ricardo B. R. Azevedo together with Christina L. Burch and colleagues from the University of Houston in Houston and the University of North Carolina at Chapel Hill, Chapel Hill, USA, decided to approach the problem in a different way. Using computer models they decided to look for the conditions that could lead to the appearance of negative epistasis in the first place.
Azevedo, Burch and colleagues knew, from earlier studies, that negative epistasis seemed to appear in populations with high robustness (robustness is the ability of a system to continue to function when experiencing genetic perturbations such as mutations). Also, it was known that a high mutation rate in a population led to increased robustness to mutation. A possibility, thought by Azevedo, Burch and colleagues, was that SR with its ability to create new genetic combinations might also act as a genetic perturbation and, therefore, lead to increased robustness to mutation.
To test this hypothesis the group of scientists used computer models simulating the evolution of asexual or sexual reproducing populations under conditions known to lead to increased robustness, and measured changes in robustness to mutation and epistasis until the populations reached equilibrium.
What the results showed was that sexual reproduction led to increased robustness to mutation in each new generation and, as a by-product, to negative epistasis. Remarkably, this showed that SR selected for conditions that favoured its own maintenance, i.e. negative epistasis. In the ASR population there was a much lower increase in genetic robustness and consequently these populations never managed to achieve negative epistasis.
These results are very interesting because they can finally start elucidating one of the big mysteries of biology: why sex persists in nature even if it seems so inefficient when compared with asexual reproduction. Azevedo, Burch and colleagues’ work shows, for the first time, that there is a direct connection between negative epistasis and sexual reproduction. This result proves that the mutational deterministic hypothesis, which claim that sex remarkable evolutionary advantage is the capacity of eliminate harmful mutations, is correct as long as all the conditions are satisfied. Now the challenge for evolutionary geneticists is to measure negative epistasis in different species.
What is also clear is that in populations with a low mutation rate, or without negative epistasis , MDH cannot, on its own, explain why SR has been maintained throughout evolution. Interestingly, this might suggest that there is more than only one major evolutionary advantage to SR. Sex remains as exciting as ever!
1 Nature 2nd March 2005
"Sexual Reproduction Selects for Robustness and Negative Epistasis in Artificial Gene Networks”
Original paper’s authors
Link to the original paper - http://www.nature.com/nature/index.html
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In collaboration with the Observatório da Ciência e do Ensino Superior (OCES)
Financed by the Fundação para a Ciência e Tecnologia (FCT) |
