Professor Daven Presgraves and Research Assistant J.P. Masly believe that they have proved a controversial evolutionary theory that credits the X chromosome with stopping the process of speciation.
Presgrave’s research involved mating two species of fruit flies (genus Drosophilia) through 15 generations, carefully tracking genes that translate into infertility among male hybrids. The team showed that 60 percent of the genes that caused infertility were located on the X chromosome, compared to the 18 percent of tracked genes on non-sex chromosomes that translated into infertility.
“There is no more debate… the large X effect is real. …Our study shows that, compared to autosomes [non-sex chromosomes], the X chromosome carries four times as many genes, causing sterility in hybrid males,” Presgraves said. “In other words, the reason the X has such a large effect on hybrid male sterility is that it simply has more sterility-causing genes than the autosomes.”
Evolutionary biologists use the term “species” to contrast populations that are reproductively isolated from one another, meaning that they cannot or will not mate. A successful mating produces viable offspring – that is, the offspring are able to mate and have offspring of their own. An unsuccessful mating occurs when the offspring is either sterile or dies before maturing.
The mule is a classical example of a sterile mating between horse and donkey. From the point of view of Professor Presgraves and other evolutionary biologists, speciation is governed by two major rules – the Haldane’s rule and the X effect.
Haldane’s rule states that when you mate two species and find that one of the two sexes is sterile, the sterile sex has an XY chromosome pairing (widely thought of as an infertile male).
The second, more controversial rule is the large X effect, which states whether or not the X chromosome plays a special role in speciation. This role would be more than that associated with any of the other autosomal or non-sex chromosomes.
“We’re interested in these rules because they apply to speciation in all animals – mammals, birds, butterflies, etc.,” Presgraves said. “If we can explain the genetic and evolutionary causes of these rules, then we can explain the origin of new species in all animals [not just sterile inviable hybrids].”
Presegraves clarified that the genes in question are not always harmful.
“An important note here – the genes that cause sterility in hybrids don’t normally cause sterility as long as they’re in the genome of their own species. They only cause problems when you move them into the genome of another species. As an analogy, computer software that works great on your Mac doesn’t usually do so well when you put it on your PC.”
The traditional view has been that the X chromosome is larger than its partner, the Y chromosome, and thus has a much larger number of genes. The Y chromosome cannot compensate due to its much smaller size. Presgraves refers to this as trying to cross-reference a pamphlet [the Y chromosome] for the same information found in an encyclopedia [the X]. He insists that this would be an impossible task.
Presgraves suggests that there is more than simple size involved in this process. He believes that the X chromosome somehow intervenes in the genes that trigger the creation of sperm in hybrid males.
Presgraves’s future research will continue to explore the mechanisms of how this is possible. By exploring these avenues, he said, we can hope to learn more about the X chromosome’s important role in driving speciation.
The Presgraves lab’s research has been published as a new study in the PloS Biology journal.
Sahay is a member of the class of 2011.
