Laboratoire Biométrie et Biologie Evolutive, Centre National de la Recherche Scientifique (CNRS), Université Lyon 1, Bâtiment Mendel, 43 boulevard du 11 novembre, 69622 Villeurbanne, France.
Am Nat. 2013 Jul;182(1):E15-24. doi: 10.1086/670612.
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.
许多昆虫携带能够操纵昆虫繁殖的细胞内细菌，从而促进细菌自身的传播。细胞质不相容性 (CI) 是这种操纵的常见形式，其中（目前尚未确定）细菌对雄性精子的修饰会导致胚胎早期死亡，除非受精卵携带来自母亲的相同细菌。未感染胚胎的死亡为感染胚胎提供了间接的选择优势，从而促进了细菌的传播。在这里，我们使用和扩展了最近开发的算法，从蚊子库蚊中推断出复杂不相容性数据背后的遗传结构。我们表明，CI 需要比以前认为的更多的遗传决定因素，并且基因产物的数量变化可能导致观察到的 CI 模式。与 CI 的群体遗传理论一致，我们的分析表明，毒素因子（诱导胚胎死亡的因子）在细菌基因组中的拷贝数比抗毒素因子（确保感染胚胎存活的因子）少。结合比较基因组学，我们的方法将为确定 CI 的遗传基础以及更一般地确定其他可以在同一框架下概念化的毒素/抗毒素系统的遗传基础提供有用的指导。
