¹Team Genetics of Adaptation, Laboratoire Génétique et Environnement, Institut des Sciences de l'Evolution (UMR CNRS 5554), Université de Montpellier II (C.C. 065), F-34095 Montpellier cedex 05, France

Correspondence: M Weill, Team Genetics of Adaptation, Laboratoire Génétique et Environnement, Institut des Sciences de l'Evolution (UMR CNRS 5554), Université de Montpellier II (C.C. 065), F-34095 Montpellier cedex 05, France. E-mail: weill@isem.univ-montp2.fr

Received 13 September 2005; Accepted 6 March 2006; Published online 26 April 2006.

Abstract

Wolbachia are maternally inherited endosymbiotic bacteria that infect many arthropod species and have evolved several different ways for manipulating their host, the most frequent being cytoplasmic incompatibility (CI). CI leads to embryo death in crosses between infected males and uninfected females, as well as in crosses between individuals infected by incompatible Wolbachia strains. In the mosquito Culex pipiens, previous studies suggested developmental variation in embryos stemming from different incompatible crosses. We have investigated this variation in different incompatible crosses. Unhatched eggs were separated into three classes based upon the developmental stage reached by the embryos. We found that incompatible crosses involving uninfected females produced only embryos whose development was arrested at a very early stage, irrespective of the Wolbachia variant infecting the male. These results differ from other host species where a developmental gradient that could reach late stages of embryogenesis or even living larvae was observed, and indicate a novel peculiarity of CI mechanism in C. pipiens. By contrast, all incompatible crosses with infected C. pipiens females produced embryos of all three classes. The proportion of embryo classes appeared to be associated with the strains involved, suggesting specific CI properties in different incompatible crosses. In addition, the contribution of parental genome was characterized in embryo classes using molecular markers for each chromosome. Embryo phenotypes appeared linked to the paternal chromosomes' contribution, as described in Drosophila simulans. However, this contribution varied according to maternal infection and independently of male factors.