Version 1
: Received: 21 April 2021 / Approved: 26 April 2021 / Online: 26 April 2021 (15:56:50 CEST)
How to cite:
Namias, A.; Sicard, M.; Weill, M.; Charlat, S. Molecular Models of Wolbachia-Induced Cytoplasmic Incompatibility Must Account for the Multiplicity of Compatibility Types.. Preprints2021, 2021040682. https://doi.org/10.20944/preprints202104.0682.v1
Namias, A.; Sicard, M.; Weill, M.; Charlat, S. Molecular Models of Wolbachia-Induced Cytoplasmic Incompatibility Must Account for the Multiplicity of Compatibility Types.. Preprints 2021, 2021040682. https://doi.org/10.20944/preprints202104.0682.v1
Namias, A.; Sicard, M.; Weill, M.; Charlat, S. Molecular Models of Wolbachia-Induced Cytoplasmic Incompatibility Must Account for the Multiplicity of Compatibility Types.. Preprints2021, 2021040682. https://doi.org/10.20944/preprints202104.0682.v1
APA Style
Namias, A., Sicard, M., Weill, M., & Charlat, S. (2021). Molecular Models of <em>Wolbachia</em>-Induced Cytoplasmic Incompatibility Must Account for the Multiplicity of Compatibility Types.. Preprints. https://doi.org/10.20944/preprints202104.0682.v1
Chicago/Turabian Style
Namias, A., Mylène Weill and Sylvain Charlat. 2021 "Molecular Models of <em>Wolbachia</em>-Induced Cytoplasmic Incompatibility Must Account for the Multiplicity of Compatibility Types." Preprints. https://doi.org/10.20944/preprints202104.0682.v1
Abstract
Wolbachia endosymbionts commonly induce cytoplasmic incompatibility, making infected males’ sperm lethal to the embryos unless these are rescued by the same bacterium, inherited from their mother. Causal genes were recently identified but two families of mechanistic models are still opposed. In the toxin-antidote model, interaction between the toxin and the antidote is required for rescuing the embryos. In host modification models, a host factor is misregulated in sperm and rescue occurs through compensation or withdrawal of this modification. While these models have been thoroughly discussed, the multiplicity of compatibility types, i.e., the existence of many mutually incompatible strains, as seen in Culex mosquitoes, has not received sufficient attention. To explain such a fact, host modification models must posit that the same embryonic defects can be induced and rescued through a large variety of host targets. Conversely, the toxin-antidote model simply accommodates this pattern through variations in the toxin-antidote interaction sites.
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
