Format

Send to

Choose Destination
Nat Microbiol. 2017 Mar 1;2:17007. doi: 10.1038/nmicrobiol.2017.7.

A Wolbachia deubiquitylating enzyme induces cytoplasmic incompatibility.

Author information

1
Department of Molecular Biophysics &Biochemistry, Yale University, 266 Whitney Avenue, New Haven, Connecticut 06520, USA.
2
Department of Molecular, Cellular, &Developmental Biology, Yale University, 266 Whitney Avenue, New Haven, Connecticut 06520, USA.

Abstract

Wolbachia are obligate intracellular bacteria1 that infect arthropods, including approximately two-thirds of insect species2. Wolbachia manipulate insect reproduction by enhancing their inheritance through the female germline. The most common alteration is cytoplasmic incompatibility (CI)3-5, where eggs from uninfected females fail to develop when fertilized by sperm from Wolbachia-infected males. By contrast, if female and male partners are both infected, embryos are viable. CI is a gene-drive mechanism impacting population structure6 and causing reproductive isolation7, but its molecular mechanism has remained unknown. We show that a Wolbachia deubiquitylating enzyme (DUB) induces CI. The CI-inducing DUB, CidB, cleaves ubiquitin from substrates and is encoded in a two-gene operon, and the other protein, CidA, binds CidB. Binding is strongest between cognate partners in cidA-cidB homologues. In transgenic Drosophila, the cidA-cidB operon mimics CI when sperm introduce it into eggs, and a catalytically inactive DUB does not induce sterility. Toxicity is recapitulated in yeast by CidB alone; this requires DUB activity but is rescued by coexpressed CidA. A paralogous operon involves a putative nuclease (CinB) rather than a DUB. Analogous binding, toxicity and rescue in yeast were observed. These results identify a CI mechanism involving interacting proteins that are secreted into germline cells by Wolbachia, and suggest new methods for insect control.

PMID:
28248294
PMCID:
PMC5336136
DOI:
10.1038/nmicrobiol.2017.7
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center