Section: New Results

On the genetic architecture of cytoplasmic incompatibility

Numerous insects carry intracellular bacteria manipulating their reproduction and thus facilitating their own spread. Cytoplasmic incompatibility (CI) is a common form of such manipulation, where a (currently uncharacterized) bacterial modification of male sperm 35 induces the early death of embryos unless the fertilized eggs carry the same bacteria, inherited from the mother. The death of uninfected embryos provides an indirect selective advantage to infected ones, thus enabling the spread of the bacteria. We used and expanded recently developed algorithms (the first being the one described in the previous item) to infer the genetic architecture underlying the complex incompatibility data from the mosquito Culex pipiens. We showed that CI requires more genetic determinants 40 than previously believed, and that quantitative variation in gene products potentially contributes to the observed CI patterns. In line with population genetic theory of CI, our analysis suggests that toxin factors (those inducing embryo death) are present in fewer copies in the bacterial genomes than antitoxin factors (those ensuring that infected embryos survive). In combination with comparative genomics, our approach will provide helpful guidance to 45 identify the genetic basis of CI, and more generally of other toxin / anti-toxin systems that can be conceptualised under the same framework. This work is currently submitted for publication. It was done in collaboration with Sylvain Charlat from the LBBE.