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Terrestrial arthropods are commonly infected with maternally inherited bacterial symbionts that cause cytoplasmic incompatibility (CI). In CI, the outcome of crosses between symbiont-infected males and uninfected females is reproductive failure, increasing the relative fitness of infected females and leading to spread of the symbiont in the host population. CI symbionts have profound impacts on host genetic structure and ecology and may lead to speciation and the rapid evolution of sex determination systems.  Cardinium hertigii , a member of the  Bacteroidetes  and symbiont of the parasitic wasp  Encarsia pergandiella , is the only known bacterium other than the  Alphaproteobacteria Wolbachia  to cause CI. Here we report the genome sequence of  Cardinium hertigii c Eper1. Comparison with the genomes of CI–inducing  Wolbachia pipientis  strains  w Mel,  w Ri, and  w Pip provides a unique opportunity to pinpoint shared proteins mediating host cell interaction, including some candidate proteins for CI that have not previously been investigated. The genome of  Cardinium  lacks all major biosynthetic pathways but harbors a complete biotin biosynthesis pathway, suggesting a potential role for  Cardinium  in host nutrition.  Cardinium  lacks known protein secretion systems but encodes a putative phage-derived secretion system distantly related to the antifeeding prophage of the entomopathogen  Serratia entomophila . Lastly, while  Cardinium  and  Wolbachia  genomes show only a functional overlap of proteins, they show no evidence of laterally transferred elements that would suggest common ancestry of CI in both lineages. Instead, comparative genomics suggests an independent evolution of CI in  Cardinium  and  Wolbachia  and provides a novel context for understanding the mechanistic basis of CI.

Comparative Genomics Suggests an Independent Origin of Cytoplasmic Incompatibility in Cardinium hertigii