Joined: July 2005
|Julie - thats actually interesting - I'm interested in the 'manipulation of host reproduction' and the game theory surrounding this. How host-specific are Wolbachia and is there a scale of host-endosymbiont interdependence between different species?|
Interesting that you should ask that. In just about every species that harbors a persistent Wolbachia infection, there seems to be a unique sequence at an easily amplifiable Wolbachia surface protein gene. We do know that horizontal transmission is possible, even though most transmission is vertical. For one thing, the most closely related infected insect species don't normally carry the most closely related bacterial strains. Wolbachia infections have been experimentally introgressed into new species; sometimes a "hybrid" between two closely related animal species is fertile if backcrossed to one of the parent species, and that's the way it's been done. There's also some evidence that parasitoids may be able to pick up the infection from their hosts, since they develop in close contact with host body tissues and fluids. Infections have also been experimentally established in insect embryos via microinjection.
There are four primary ways in which Wolbachia biases host reproduction towards making lots of infected daughters:
Feminization (F). Infected genetic males develop as females. This one's known only from some terrestrial crustaceans, and probably depends on a bacterial effect on ZW sex determination pathways. (ZW sex determination is sort of the opposite of XY. Females in these species are ZW, and males are ZZ.)
Parthenogenesis induction (PI): Infected females can produce daughters by gamete duplication, without having to mate. This is best characterized in some parasitoid wasps. Interestingly, the true wasps, bees, and ants have a sex-determination system with which classic PI just can't work. (This is another field of research for me, but I'll control myself.) :-)
Cytoplasmic incompatibility (CI): Infected females can mate successfully with any male, but if an uninfected female mates with an infected male, her embryos won't develop. This means that infected females have better mating prospects, and thus higher reproductive success. This is known in many insects, especially in numerous Drosophila species.
Male-killing (MK): Some or all male embryos of infected mothers die, so that their daughters get more resources. Since this doesn't imply parthenogenesis, MK infections tends to exist at intermediate frequencies in a trade-off situation; if it swept completely through the population, an MK infection would cause host extinction through loss of mating opportunities.
There are other adaptations known, though, too numerous to list here. There's no easy way to correlate related strains with reproductive effects; the infection "phenotype" seems to be a product of the host-symbiont interaction rather than of the bacteria themselves. Incidentally, different Wolbachia strains infect nematodes, and in this phylum, the host and symbiont phylogenies match up pretty well!
I can go on about this for hours, so I'll quit before everyone is completely reeling ....
|Any snappy references?|
I'm really an applied molecular ecologist rather than a theoretical type, so I don't have an at-my-figurative-fingertips list, but a quick web search turned up this one that at least mentions Wolbachia dynamics:
Hammerstein, Peter. 2005. Strategic analysis in evolutionary genetics and the theory of games. Journal of Genetics 84: 7-12.
Hope this helps,