On the Genetic Architecture of Cytoplasmic Incompatibility
Inference from Phenotypic Data
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Date
2013-07
Publication Type
Journal Article
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yes
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Abstract
Numerous insects carry intracellular bacteria that manipulate the insects' reproduction and thus facilitate their own spread. Cytoplasmic incompatibility (CI) is a common form of such manipulation, where a (currently uncharacterized) bacterial modification of male sperm induces the early death of embryos unless the fertilized eggs carry the same bacteria, inherited from the mother. The death of uninfected embryos provides an indirect selective advantage to infected ones, thus enabling the spread of the bacteria. Here we use and expand recently developed algorithms to infer the genetic architecture underlying the complex incompatibility data from the mosquito Culex pipiens. We show that CI requires more genetic determinants than previously believed and that quantitative variation in gene products potentially contributes to the observed CI patterns. In line with population genetic theory of CI, our analysis suggests that toxin factors (those inducing embryo death) are present in fewer copies in the bacterial genomes than antitoxin factors (those ensuring that infected embryos survive). In combination with comparative genomics, our approach will provide helpful guidance to identify the genetic basis of CI and more generally of other toxin/antitoxin systems that can be conceptualized under the same framework. © 2013 by The University of Chicago.
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published
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Volume
182 (1)
Pages / Article No.
E15 - E24
Publisher
University of Chicago Press
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Subject
Wolbachia; Cytoplasmic incompatibility; Model; Toxin-antitoxin systems; Gene-for-gene systems
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Submitted 23 May 2012, Accepted 7 January 2013, Published online 7 May 2013.