Wolbachia are maternally transmitted, intracellular bacteria that can often selfishly spread through arthropod populations via cytoplasmic incompatibility (CI). CI manifests as embryonic death when males expressing prophage WO genes
cifA and
cifB mate with uninfected females or females harboring an incompatible
Wolbachia strain. Females with a compatible
cifA-expressing strain rescue CI. Thus,
cif-mediated CI confers a relative fitness advantage to females transmitting
Wolbachia. However, whether
cif sequence variation underpins incompatibilities between
Wolbachia strains and variation in CI penetrance remains unknown. Here, we engineer
Drosophila melanogaster to transgenically express cognate and non-cognate
cif homologs and assess their CI and rescue capability. Cognate expression revealed that
cifA;B native to
D. melanogaster causes strong CI, and cognate
cifA;B homologs from two other
Drosophila-associated
Wolbachia cause weak transgenic CI, including the first demonstration of phylogenetic type 2
cifA;B CI. Intriguingly, non-cognate expression of
cifA and
cifB alleles from different strains revealed that
cifA homologs generally contribute to strong transgenic CI and interchangeable rescue despite their evolutionary divergence, and
cifB genetic divergence contributes to weak or no transgenic CI. Finally, we find that a type 1
cifA can rescue CI caused by a genetically divergent type 2
cifA;B in a manner consistent with unidirectional incompatibility. By genetically dissecting individual CI functions for type 1 and 2
cifA and
cifB, this work illuminates new relationships between
cif genotype and CI phenotype. We discuss the relevance of these findings to CI’s genetic basis, phenotypic variation patterns, and mechanism.
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