In the prime of his life, Aneil Agrawal is plagued by a question most young people never contemplate: Why have sex at all? It's not a personal issue. It's a biological one.
"Evolutionary theory predicts that females should reproduce asexually, rather than sexually," says Dr. Agrawal, winner of the 2004 NSERC Howard Alper Postdoctoral Prize. "Yet when we look around in the biological world there's a lot of sex going on. So this is a mystery. How do we explain the force that must be favouring sex?"
Dr. Agrawal is a rising star in the field of evolutionary theory, where math, statistics and biology meet to solve evolutionary riddles. Much of his thinking focuses on why we live in a world in which Noah had to load the ark by twos. While the answers might seem obvious in our Sex in the City-obsessed culture, his probing is overturning long-held assumptions about the genetic benefits of cohabitation.
One of the key explanations for the prevalence of mating rather than simply dividing is the presumed benefits of genetic mixing. Prior to a sex cell splitting to produce two sperms or eggs, its paired chromosomes swap bits of genetic material in an act called recombination. Thus, the offspring gets a unique genetic package from each parent.
"But it's not obvious whether recombination is a good or a bad thing," says Dr. Agrawal, who's a postdoctoral fellow in the lab of University of British Columbia (UBC) evolutionary biologist Dr. Sarah Otto, a former NSERC Steacie Fellow. "Recombination is helpful when it rearranges poor gene combinations into good ones, but harmful when it messes up what's already working."
Some evolutionary biologists have suggested that recombination might not be so mysterious if it is "plastic." In this context, the extent of recombination varies between individuals and populations depending on their physical condition. If an individual's succeeding, there's little recombination. If it's highly stressed, there's more.
There's already theoretical evidence that this makes sense for haploid organisms, those whose cells contain only a single version of each chromosome. And since the early 1900s there's been experimental evidence with plants, mice and fruit flies that this is also the case with diploid organisms – those, including humans, that have two copies of each chromosome, one from mom and the other from dad.
However, through mathematical modelling Dr. Agrawal, in collaboration with Dr. Lilach Hadany (Stanford) and Dr. Sarah Otto (UBC), has recently shown that the theoretical reasoning that makes plastic recombination beneficial for haploids doesn't extend to their paired-chromosome relatives.
"It doesn't work at all for diploids," says Dr. Agrawal, of the as yet unpublished results. "So we're left in a mystery here in that there's empirical data showing that this phenomenon exists in diploids, but we've found no theoretical basis for it."
To help solve this sexual quandary Dr. Agrawal – who'll start a position as an assistant professor in the Department of Zoology at the University of Toronto in July – is currently leading two experiments to examine whether having a "bad" genotype does in fact increase recombination in diploid organisms.
In one experiment, fruit flies are being engineered to have mutations on their second chromosome, and the extent of recombination will be measured on the third chromosome.
In the second, he will compare the recombination rates of two populations of flies, one adapted to cold, the other to warm conditions. Members of each group will be placed in both warm and cool environments. Dr. Agrawal's prediction is that flies with genotypes adapted to a given environment will have less recombination in that environment than flies with genotypes adapted to the alternative environment.
"It's really nice to be able to say why something as fundamental as sex occurs," says Dr. Agrawal. "We can't do that with diploids and plastic recombination yet, but we can at least say what it's not due to."