Affiliation:
1. Department of Molecular Biophysics and Biochemistry and Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, Connecticut, USA;
Abstract
Among endosymbiotic bacteria living within eukaryotic cells, Wolbachia is exceptionally widespread, particularly in arthropods. Inherited through the female germline, it has evolved ways to increase the fraction of bacterially infected offspring by inducing parthenogenesis, feminization, male killing, or, most commonly, cytoplasmic incompatibility (CI). In CI, Wolbachia infection of males causes embryonic lethality unless they mate with similarly infected females, creating a relative reproductive advantage for infected females. A set of related Wolbachia bicistronic operons encodes the CI-inducing factors. The downstream gene encodes a deubiquitylase or nuclease and is responsible for CI induction by males, while the upstream product when expressed in females binds its sperm-introduced cognate partner and rescues viability. Both toxin-antidote and host-modification mechanisms have been proposed to explain CI. Interestingly, male killing by either Spiroplasma or Wolbachia endosymbionts involves deubiquitylases as well. Interference with the host ubiquitin system may therefore be a common theme among endosymbiont-mediated reproductive alterations.