Aude Ligier, Daniele Arnoldi, Sandra Unal, Rudy Caparros, Marco Perriat-Sanguinet, Beniamino Caputo, Mathieu Sicard, Mylène Weill, Manon Bonneau, Institut des Sciences de l'Evolution de Montpellier (UMR ISEM), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université de Montpellier (UM)-Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-Centre National de la Recherche Scientifique (CNRS)-Institut de recherche pour le développement [IRD] : UR226, Instituto Gulbenkian de Ciência [Oeiras] (IGC), Fundação Calouste Gulbenkian, Institut Pasteur, Fondation Cenci Bolognetti - Istituto Pasteur Italia, Fondazione Cenci Bolognetti, Réseau International des Instituts Pasteur (RIIP), Université de Liège, Centro Ricerca e Innovazione - Research and Innovation Centre [FEM - Italie], Fondazione Edmund Mach - Edmund Mach Foundation [Italie] (FEM), This work was funded by the French ANR (project 'CIAWOL' ANR‐16‐ CE02‐0006‐01)., We would like to thank Bertrand Lelièvre for his help with mosquito sampling and Dr Nicole Pasteur for helpful comments on the manuscript. We thank Fabienne Justy for her help in RNA extraction and Dr Laurent Marivaux for the use of the stereomicroscope funded by PALASIAFRICA ANR/ERC. We also thank Dr Philippe Clair for his help with the real‐time quantitative PCR experiments performed at the technical facility of the qPCR Haut Debit (qPHD) Montpellier génomiX platform. Sequencing data were generated on the GENSEQ platform of the technical facilities of the LabEX Centre Méditerranéen de l'Environnement et de la Biodiversité. The CI status of crosses was determined with help of the CytoEvol facilities of UMR ISEM ‐ CBGP of the LabEx CeMEB., ANR-16-CE02-0006,CIAWOL,Bases moléculaire et cellulaire de la diversité phénotypique de l'incompatibilté cytoplasmique chez les insectes(2016), Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-École Pratique des Hautes Études (EPHE), and Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université de Montpellier (UM)-Institut de recherche pour le développement [IRD] : UR226-Centre National de la Recherche Scientifique (CNRS)
International audience; Endosymbiotic Wolbachia bacteria are, to date, considered the most widespread symbionts in arthropods and are the cornerstone of major biological control strategies. Such a high prevalence is based on the ability of Wolbachia to manipulate their hosts' reproduction. One manipulation called cytoplasmic incompatibility (CI) is based on the death of the embryos generated by crosses between infected males and uninfected females or between individuals infected with incompatible Wolbachia strains. CI can be seen as a modification-rescue system (or mod-resc) in which paternal Wolbachia produce mod factors, inducing embryonic defects, unless the maternal Wolbachia produce compatible resc factors. Transgenic experiments in Drosophila melanogaster and Saccharomyces cerevisiae converged towards a model where the cidB Wolbachia gene is involved in the mod function while cidA is involved in the resc function. However, as cidA expression in Drosophila males was required to observe CI, it has been proposed that cidA could be involved in both resc and mod functions. A recent correlative study in natural Culex pipiens mosquito populations has revealed an association between specific cidA and cidB variations and changes in mod phenotype, also suggesting a role for both these genes in mod diversity. Here, by studying cidA and cidB genomic repertoires of individuals from newly sampled natural C. pipiens populations harbouring wPipIV strains from North Italy, we reinforce the link between cidB variation and mod phenotype variation fostering the involvement of cidB in the mod phenotype diversity. However, no association between any cidA variants or combination of cidA variants and mod phenotype variation was observed. Taken together our results in natural C. pipiens populations do not support the involvement of cidA in mod phenotype variation.