No abstract

Male-killing bacteria are cytoplasmic sex-ratio distorters that are transmitted vertically through females of their insect hosts. The killing of male hosts by their bacteria is thought to be an adaptive bacterial trait because it augments the fitness of female hosts carrying clonal relatives of those bacteria. Here we attempt to explain observations of multiple male-killers in natural host populations. First we show that such male-killer polymorphism cannot be explained by a classical model of male-killing. We then show that more complicated models incorporating the evolution of resistance in hosts can explain male-killer polymorphism. However, this is only likely if resistance genes are very costly. We also consider the long-term evolutionary dynamics of male-killers, and show that evolution towards progressively more 'efficient' male-killers can be thwarted by the appearance of host resistance. The presence of a resistance gene can allow a less efficient male-killer to outcompete its rival and hence reverse the trend towards more efficient transmission and reduced metabolic load on the host.

In lekking species, intense directional selection is applied to aspects of the male genotype by female choice. Under conventional quantitative genetics theory, the expectation is that this will lead to a rapid loss in additive genetic variance for the trait in question. However, despite female choice, male variation is maintained and hence it pays females to continue choosing. This has been termed the`paradox of the lek'. Here we present a theoretical analysis of a putative sex-role-reversed lek in the butter£y Acraea encedon. Sex-role reversal appears to have come about because of infection with a male-killing Wolbachia. The bacterium is highly prevalent in some populations, such that there is a dearth of males. Receptive females form dense aggregations, and it has been suggested that males preferentially select females uninfected with the bacterium. As with more conventional systems, this presents a theoretical problem exactly analogous to the lek paradox, namely, what maintains female variation and hence why do males continue to choose ? We model the evolution of a male choice gene that allows discrimination between infected and uninfected females, and show that the stable maintenance of both female variation and male choice is likely, so long as males make mistakes when discriminating between females. Furthermore, our model allows the maintenance, in a panmictic population, of a male killer that is perfectly transmitted. This is the ¢rst model to allow this result, and may explain the long-term persistence of a male killer in Hypolimnas bolina.

Maternally transmitted bacteria that kill male hosts early in their development are found in many insects. These parasites typically infect 1-30% of wild females, but in a few species of insects, prevalences exceed 95%. We investigated one such case in the butterfly Acraea encedon, which is infected with a male-killing Wolbachia bacterium. We measured three key parameters that affect the prevalence of the parasite: transmission efficiency, rate of survival of infected males, and the direct cost of infection. We observed that all wild females transmit the bacterium to all their offspring and that all infected males die in wild populations. We were unable to detect any physiological cost to infection in lab culture. These observations explain the high prevalence of the A. encedon male killer, as theory predicts that under these conditions the parasite will spread to fixation. This will occur provided the death of males provides some benefit to the surviving infected females. The problem therefore becomes why the bacterium has not reached fixation and driven the butterfly extinct due to the shortage of males. We therefore investigated whether males choose to mate with uninfected rather than infected females, as this would prevent the bacterium from reaching fixation. We tested this hypothesis in the "lekking swarms" of virgin females found in the most female-biased populations, and were unable to detect any evidence of mate choice. In conclusion, this male killer has spread to high prevalence because it has a high transmission efficiency and low cost, but the factors maintaining uninfected females in the population remain unknown.

Why are sperm small and eggs large ? The dominant explanation for the evolution of gamete size dimorphism envisages two opposing selection pressures acting on gamete size: small gametes are favoured because many can be produced, whereas large gametes contribute to a large zygote with consequently increased survival chances. This model predicts disruptive selection on gamete size (i.e. selection for anisogamy) if increases in zygote size confer disproportional increases in ¢tness (at least over part of its size range). It therefore predicts that increases in adult size should be accompanied by stronger selection for anisogamy. Using data from the green algal order Volvocales, we provide the ¢rst phylogenetically controlled test of the model's predictions using a published phylogeny and a new phylogeny derived by a di¡erent method. The predictions that larger organisms should (i) have a greater degree of gamete dimorphism and (ii) have larger eggs are broadly upheld. However, the results are highly sensitive to the phylogeny and the mode of analysis used.