Credit: Eric Marechal
Sex—it gives us diseases, sucks away our energy, clouds our judgment and doesn’t even transfer our genes that efficiently anyway. So why have humans and most other animals evolved this bizarre, slightly dirty quirk of sexual reproduction? Why haven’t we all taken Woody Allen‘s advice, and evolved to reproduce with someone we love, instead?
Evolutionary biologists have pondered this question since the late 19th century, when German biologist August Weismann proposed that sexual reproduction evolved to create variety amongst siblings. A new understanding of genomics in the 20th century led to refinements of his theory, and allowed new ones to emerge. The so-called Red Queen hypothesis, named after a character from Lewis Carroll‘s Through the Looking Glass, for example, explains sex as an adaptation that helps sexual reproducers resist parasites. According to this hypothesis, sexual reproduction—which can create variation from generation to generation evolved to allow species to develop adaptations to avoid their specific parasites.
Another explanation, the mutational deterministic hypothesis (MDH) proposed by Alexey Kondrashov in the late 1980s, posits that sex works to combine deleterious mutations. As generations pass, the mutations act upon one another in an exponentially harmful build-up that finally works to kill the organism, killing the mutations in the process. In other words, certain lineages act as mutation traps, eventually being eliminated to protect the rest of the species.
While MDH is probably the most widely accepted theory that attempts to describe sexual reproduction’s prevalence, it has never been proven. Recently, University of Houston biologist Ricardo Azevedo created a computer model of genetic interactions to study the evolution of a simple organism under several sets of conditions. He and colleague Christina Burch of the University of North Carolina determined that sexual reproduction is self-reinforcing, and that it can lead to a genetic phenomenon called negative epistasis, an exponentially harmful accumulation of mutations that’s a proposed precondition of MDH. While this research does not provide a conclusive proof for MDH, it may help future scientists solve the enduring mystery of sexual reproduction’s evolution.
Seed spoke with Azevedo about his research, and asked him the burning question: Why on Earth aren’t we all asexual mutants?
Can you explain, in evolutionary terms, why sex is such a problem?
Males go out of their way to persuade females to mate with them. All this expends a lot of energy and a lot of resources, and so on a strictly utilitarian view, you would think that asexuals would have a direct advantage.
Courtesy of Ricardo Azevedo
So what would the alternative be?
If you imagine, for example, in a population like the human population, if there was a mutation that turned a female into an asexually reproducing female that could just have female offspring without sexual encounters, then that single individual would start a clone of females that would, per capita, have twice the reproductive rate of the normal human population. You would think that sexual populations could be invaded by asexual mutants, and that sexuality could be displaced by asexuals.
But it hasn’t, clearly. Or if it has, no one’s told me yet.
No, [asexuality] seems to be a dead end, somehow, evolutionarily. When asexuals appear, they don’t last very long. They can have a short-term advantage, maybe, and run for a little while. But at some point something happens to them and they disappear. If the MDH or a similar theory is correct, they simply accumulate harmful mutations and die out.
So one theory for why asexuals aren’t as selectively successful as sexuals is MDH. I know it’s based on the assumption that negative epistasis will affect an organism. What is negative epistasis?
RA: Imagine that on average a harmful mutation will decrease fitness by about 5%. If you imagine now an organism with successive rounds of harmful mutation, you’d imagine that if the mutations don’t have anything to do with each other, then every time you add the next harmful mutation, you’ll just decrease fitness by another 5%. The first knocks it down by 5%, the second knocks it down by another 5%, and so on. It just keeps going that way. The alternative then is if the mutations interact with each other. Negative epistasis is the case where, as you add more and more mutations, the effects become progressively worse. So first you lose five, the second you lose 10, the third you lose 15, and it just keeps getting worse. So after a few rounds of mutations, you’re essentially dead, because the mutations accumulate.
So according to MDH, sex has evolved to isolate and destroy mutations. How does this make us more effective than the asexual mutants?
One of the things that sexual reproduction can do is produce individuals every generation that concentrate many mutations because sex can recombine different genomes. Asexuals find it very difficult to fight against [mutations], because they cannot recombine and so they cannot produce these individuals with either fewer mutations or more mutations. They can only live with what they have.
How has your research helped provide evidence for MDH?
[Our results showed that] in conditions that select for insensitivity to mutation, sexual reproduction adds to this selection and then leads to the evolution of negative epistasis as a byproduct. So, if these conditions are realistic in nature, it suggests that negative epistasis should be out there, in many organisms and in many bases.
Finally, what should all of this mean about how humans view sex, in a social way? Does this make you frightened of sex?
No, not based on our work, except perhaps, in a strictly scientific sense. The origin and maintenance of sex is still a very difficult question that will not be solved easily. One thing to note is that, in an evolutionary sense, humans and other mammals have no choice in the matter; due to genomic imprinting, it’s unlikely that we’ll ever be taken over by asexual clones.
Originally published April 11, 2006
