On the Genetic Architecture of Cytoplasmic Incompatibility: Inference from Phenotypic Data
On the Genetic Architecture of Cytoplasmic Incompatibility: Inference from Phenotypic Data
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DOI：
10.1086/670612
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发表时间：
2013-07-01
影响因子：
2.9
通讯作者：
Charlat, Sylvain
中科院分区：
文献类型：
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作者：
Nor, Igor;Engelstaedter, Jan;Charlat, Sylvain
许多昆虫携带胞内细菌，这些细菌操纵昆虫的繁殖，从而促进它们自己的传播。细胞质不相容（Cytoplasmic incompatibility， CI）是这种操纵的一种常见形式，即对男性精子进行（目前尚未确定的）细菌修饰，导致胚胎过早死亡，除非受精卵携带从母体遗传来的相同细菌。未受感染的胚胎的死亡为受感染的胚胎提供了间接的选择优势，从而使细菌得以传播。在这里，我们使用并扩展了最近开发的算法来推断来自蚊子库蚊的复杂不相容数据的遗传结构。我们表明CI需要比以前认为的更多的遗传决定因素，基因产物的定量变化可能有助于观察到的CI模式。根据CI的群体遗传理论，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少于抗毒素因子（确保受感染胚胎存活的因子）。结合比较基因组学，我们的方法将提供有用的指导，以确定CI的遗传基础，更广泛地说，其他毒素/抗毒素系统可以在相同的框架下概念化。
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.