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Cytoplasmic incompatibility associated with Wolbachia strains differing in the presence of cif genes
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  • Jonathan Parrett,
  • Józefina Wasilewska,
  • Karolina Przesmycka,
  • Sebastian Chmielewski,
  • Matthias Scholz,
  • Jacek Radwan
Jonathan Parrett
Adam Mickiewicz University Faculty of Biology

Corresponding Author:[email protected]

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Józefina Wasilewska
Adam Mickiewicz University Faculty of Biology
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Karolina Przesmycka
Adam Mickiewicz University
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Sebastian Chmielewski
Adam Mickiewicz University Faculty of Biology
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Matthias Scholz
Fondazione Edmund Mach Istituto Agrario di San Michele all'Adige
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Jacek Radwan
Adam Mickiewicz University Faculty of Biology
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Abstract

Wolbachia is a widespread bacterial endosymbiont and its maternal transmission favours the selfish manipulation of host reproduction to increases in frequency. One such manipulation is cytoplasmic incompatibility (CI), where uninfected female’s eggs fail to hatch when fertilised by an infected male. If variation in infection rates and CI strength exist, Wolbachia induced CI may reduce gene-flow between populations. Here, we investigate CI between three populations of the bulb mite, Rhizoglyphus robini. Our crosses and PCR screening for Wolbachia of populations with and without antibiotic curing provide evidence that one population infected with Wolbachia induces and rescues CI: when males are mated to females either from an uninfected population or from another population infected with Wolbachia the majority of eggs fail to hatch, the latter suggesting that different Wolbachia strains infect different populations. By assembling draft Wolbachia genomes using a metagenome assembly approach, we find that Wolbachia assemblies are almost identical in aligned regions, but also find evidence for possible structural variation by performing coverage analysis. This structural variation appears to be linked phage regions and the presence/absence of “cif-like” genes, in a pattern consistent with the observed CI phenotype. Cif genes have previously be shown to be causal in inducing and rescuing CI in other species. The causal mechanisms for this structural variation remains unknown. Interestingly, we find a large number of hybrid males inheriting the CI inducing Wolbachia strain, do not themselves induce CI. We suggest this pattern is likely associated with host variant that acts to suppress CI.