1932

Abstract

Among endosymbiotic bacteria living within eukaryotic cells, 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, 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 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 or endosymbionts involves deubiquitylases as well. Interference with the host ubiquitin system may therefore be a common theme among endosymbiont-mediated reproductive alterations.

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2023-09-15
2024-05-02
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