Scientists have found the most convincing evidence yet that a parasite can contribute to splitting a species in two, thanks to a phenomenon in which a wasp's damaged sperm can be "rescued" or fixed only by mating with particular females.
A bacterium called Wolbachia prevents the successful development of embryos in matings between two very closely related wasp species that could otherwise produce viable offspring.
In today's issue of Nature, University of Rochester researchers show that the bacterium's species-splitting effect came before any other in the wasps, strongly suggesting that the parasite accelerated the natural evolution of the insect.
The research was conducted by two graduate students, Seth Bordenstein and Patrick O'Hara, and led by John Werren, professor of biology.
Wolbachia propagates itself in an unusual manner: Instead of merely helping its host compete against non-infected hosts, as many parasites do, Wolbachia actively seeks to eliminate non-infected hosts by stopping them from reproducing.
To do this, the parasite alters the sperm of its male host, rendering it infertile when paired with an uninfected female. If, however, the male mates with an infected female, the damaged reproductive cells are "rescued" by the female's parasite.
It's as if the bacterium encodes the sperm cell, rendering it useless unless it encounters the de-coding bacterium from another infected wasp. The result is that infected males can only impregnate other infected females, not uninfected ones, making it difficult for uninfected females to find a compatible mate.
The trickery is part of a wider system that assures that as many wasps as possible will pass Wolbachia on to the next generation. Infected males can have offspring only with infected females, and infected females automatically pass the infection on to all their offspring.
The only possibility for producing uninfected offspring is for two uninfected wasps to mate.
"This is the best evidence of a parasite contributing to speciation that we've seen," says Werren. "Splitting a species in two is probably just a side effect of the bacteria's reproductive method, of their way of eliminating non-infected hosts."
A consequence of this method of eliminating the non-infected appears to be that the host species is more susceptible to splitting into two species.
The two species of wasp that Werren studied can actually interbreed if given an antibiotic to kill the Wolbachia.
"The exact role of Wolbachia in speciation is a matter of current debate," says Werren. "We're not claiming that Wolbachia are solely keeping the two wasp species reproductively separated in nature, but we have shown that the ability of the bacterium to alter the insect's reproduction predates other genetic reproductive barriers. That supports the argument that Wolbachia can promote host speciation."
Bordenstein, O'Hara and Werren needed to look at the numerous genetic barriers that kept the species from interbreeding and determine which one came first.
They found little difference in the mating rituals and preferences of the two species, suggesting that those were not enough in themselves to force speciation. Also, hybrids of the two species were not sterile -- an early sign of speciation -- and the hybrids were relatively healthy.
In contrast, the presence of Wolbachia was the single highest barrier to the interbreeding of the two species, and thus, it is likely the oldest barrier.
Wolbachia infects as much as 20 percent of all insect species, and tends to infect large percentages of the individuals in those species. It was first noticed more than 50 years ago when scientists noted that some species of mosquitoes could interbreed when given antibiotics.
In the 1970s, researchers found that a bacterium was responsible, and there has been speculation ever since about whether the bacterium caused speciation of its host, or merely enhanced it.
"Our findings strongly suggest that Wolbachia was not just a bystander in the evolution of these wasps," says Werren. "It looks like this parasite played an active role."
The research was funded by the National Science Foundation. - By Jonathan Sherwood
[Contact: Jonathan Sherwood]