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Publication
One prophage WO gene rescues cytoplasmic incompatibility in Drosophila
melanogaster.
Authors Shropshire JD, On J, Layton EM, Zhou H, Bordenstein SR
Submitted By Submitted Externally on 5/25/2018
Status Published
Journal Proceedings of the National Academy of Sciences of the United States of America
Year 2018
Date Published 5/1/2018
Volume : Pages 115 : 4987 - 4991
PubMed Reference 29686091
Abstract Wolbachia are maternally inherited, intracellular bacteria at the forefront of
vector control efforts to curb arbovirus transmission. In international field
trials, the cytoplasmic incompatibility (CI) drive system of wMel Wolbachia is
deployed to replace target vector populations, whereby a Wolbachia-induced
modification of the sperm genome kills embryos. However, Wolbachia in the embryo
rescue the sperm genome impairment, and therefore CI results in a strong fitness
advantage for infected females that transmit the bacteria to offspring. The two
genes responsible for the wMel-induced sperm modification of CI, cifA and cifB,
were recently identified in the eukaryotic association module of prophage WO,
but the genetic basis of rescue is unresolved. Here we use transgenic and
cytological approaches to demonstrate that maternal cifA expression
independently rescues CI and nullifies embryonic death caused by wMel Wolbachia
in Drosophila melanogaster Discovery of cifA as the rescue gene and previously
one of two CI induction genes establishes a "Two-by-One" model that underpins
the genetic basis of CI. Results highlight the central role of prophage WO in
shaping Wolbachia phenotypes that are significant to arthropod evolution and
vector control.





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