The first lab I worked in was a fruit fly lab. As a budding mammalogist, this wasn’t the most optimal environment, but it had its advantages. I learned to work with flies, and the advantages of model systems. I learned to clean glassware with speed and grace. I learned that science involves a lot of failure. And I learned about Wolbachia (Tim Karr, mentioned in that article, was the lab’s head).
If Wolbachia lives inside a female insect, it can infect her eggs. When those eggs hatch and mature into adult insects, they will be infected by Wolbachia as well. But if Wolbachia should find itself in a male, it has reached a dead end. It cannot infect sperm cells, and thus it has no escape from a male host. When a male host dies, Wolbachia dies as well.
Wolbachia’s solution: kill the males before they kill you.
In many species, Wolbachia is lethal to male embryos.
In our fruit flies, however, it was even trickier.
Killing your host is such a bad practice. What our flies and their symbiotes did was more gentle, but just as effective for the bacteria. Infected females could produce offspring from any mating, but infected males could only produce fertile eggs with infected females. What’s called cytoplasmic incompatibility prevented them from successfully fertilizing uninfected females. One of the important discoveries from the lab had been that the same phenomenon worked between different strains of Wolbachia. A population infected with a strain from California couldn’t fertilize flies infected with a strain from Hawaii.
The research project I was working on involved a fairly obvious question: How does Wolbachia remain in the population?
Whether it kills the males or makes them less fertile, it is still making infected individuals less fit, and you ought to see the infected flies die out. That the infection remains at a stable level in the population suggests that there’s some countervailing benefit to infection.
When the bacteria enter an egg cell, they bring various proteins across. The theory was that those proteins, which were known to protect other proteins against sudden changes in temperature, might be released into the host cell and protect it against heat. My job was to put eggs at a known age into a big vat of hot water and see whether more infected eggs or uninfected eggs got killed.
At that stage and at that temperature, we found no difference. A summer’s work and nothing especially noteworthy to show for it. It suggested a range of new questions: different aged eggs, different temperatures, different amounts of time in the bath. But I couldn’t quite get myself worked up about those new experiments, so I went on to a study of rodent genitalia. I got interesting results, and somehow or other, here I am.
Wolbachia remains interesting to me, though not for its cytoplasmic effects, nor for the arms race Zimmer describes between male killing and the males in question. In some species of insect, Wolbachia produces hermaphrodites or gender switches. The advantage is the same, make the hosts that reproduce be the ones that produce infected eggs.
The example helps us understand that sex, something that is highly genetically fixed in most familiar species, is quite labile in many other species. You’ll often hear creationists argue that the evolution of sex must have been some high barrier to cross, but that assumes a level of sexual determination that isn’t characteristic of most of the animal (or plant) world. Male and female mammals are quite different for genetic reasons, but male and female mosquitoes are just one bacterium apart.
Some reptile sexes are a few degrees of temperature apart at the right point in egg development. Some mollusk sexes are a few months apart, since they develop from one sex to the next.
If I learned nothing else from my summer of the flies, it’s that biology is tricky, and sex doubly so.