Wolbachia与昆虫精卵细胞质不亲和

Wolbachia是广泛分布在昆虫体内的一类共生菌,能通过多种机制调节宿主的生殖方式,包括诱导宿主精卵细胞质不亲和(CI)、孤雌生殖、雌性化、杀雄等,其中细胞质不亲和为最普遍的表型,即感染Wolbachia的雄性和未感染或感染不同品系Wolbachia的雌性宿主交配后,受精卵不能正常发育,在胚胎期死亡。多数CI胚胎在第1次分裂时,来自父本的染色质浓缩缺陷,导致父本遗传物质无法正常分配到子细胞中,因而引起胚胎死亡。守门员模型认为,产生CI可能需要有两种因子,其中之一使得精子发生修饰改变,导致受精后雄性原核发育滞后。第2种因子可能与Wolbachia的原噬菌体有关,在胚胎发育后期导致胚胎死亡。近期的研究已发现,在Wolbachia感染的宿主中,一些与生殖细胞发生和繁殖相关基因的表达发生了显著改变,Wolbachia可能因此对宿主的生殖产生重大影响,进而导致CI的产生。本文主要综述了CI的细胞学表型、解释CI的模型及其分子机理,向读者展示一个小小的细菌是如何通过精妙的策略影响昆虫宿主的繁殖,从而实现其自身的生存和传播的。

Wolbachia induced cytoplasmic incompatibility in insects

Wolbachia are endosymbionts that infect the majority of insect species. Their successful spread is in large part attributed to their ability to manipulate reproduction in their hosts by such means as inducing sperm-egg cytoplasmic incompatibility（CI）, parthogenesis, feminization and male killing. CI is the most common phenotype, which is expressed as embryonic lethality when Wolbachia-infected males mate with uninfected females or with females infected with a different Wolbachia strain. Most CI embryos show defects in paternal chromosome condensation, resulting in paternal ＂diffused chromatin＂ next to properly condensed female chromosomes during metaphase of the first mitotic division. The embryos die due to abnormal segregation of paternal chromatin during the first mitosis producing aneuploid daughter nuclei. Based on the new goalkeeper-model, two factors are involved in the differential generation of CI in crosses between and among infected and uninfected mating partners. One involves the mistiming of cell cycle events and the other is likely related to the Wolbachia prophage and late stage embryonic lethality. Recent studies have shown that Wolbachia infection significantly changes the expression of a series of genes. Some of these are associated with gametogenesis and reproduction, probably thus leading to CI occurrence. Here we present an overview of the cytological phenotypes in CI embryos, the models for explaining CI and the molecular mechanisms underlying CI.