Wolbachia are Gram‐negative endosymbionts that are known to cause embryonic lethality when infected male insects mate with uninfected females or with females carrying a different strain of Wolbachia, a situation characterized as cytoplasmic incompatibility (CI). However, the mechanism of CI is not yet fully understood, although recent studies on Drosophila melanogaster have achieved great progress. Here, we found that Wolbachia infection caused changes in the expressions of several immunity‐related genes, including significant upregulation of kenny (key), in the testes of D. melanogaster. Overexpression of key in fly testes led to a significant decrease in egg hatch rates when these flies mate with wild‐type females. Wolbachia‐infected females could rescue this embryonic lethality. Furthermore, in key overexpressing testes terminal deoxynucleotidyl transferase‐mediated dUTP‐biotin nick‐end labeling signal was significantly stronger than in the control testes, and the level of reactive oxygen species was significantly increased. Overexpression of key also resulted in alterations of some other immunity‐related gene expressions, including the downregulation of Zn72D. Knockdown of Zn72D in fly testes also led to a significant decrease in egg hatch rates. These results suggest that Wolbachia might induce the defect in male host fertility by immunity‐related pathways and thus cause an oxidative damage and cell death in male testes.

中文翻译：

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沃尔巴克氏体诱导的睾丸中肯尼基因的表达影响黑腹果蝇的雄性生育能力

Wolbachia 是革兰氏阴性内共生菌，已知当受感染的雄性昆虫与未受感染的雌性或携带不同 Wolbachia 菌株的雌性交配时会导致胚胎致死，这种情况的特征是细胞质不相容性 (CI)。然而，尽管最近对黑腹果蝇的研究取得了很大进展，但CI的机制尚未完全清楚。在这里，我们发现 Wolbachia 感染导致黑腹果蝇睾丸中几种免疫相关基因的表达发生变化，包括 kenny (key) 的显着上调。当这些果蝇与野生型雌性果蝇交配时，果蝇睾丸中 key 的过度表达导致卵孵化率显着降低。Wolbachia 感染的雌性可以挽救这种胚胎致死率。此外，在关键过表达的睾丸中，末端脱氧核苷酸转移酶介导的 dUTP-生物素缺口末端标记信号明显强于对照睾丸，活性氧水平显着增加。key 的过度表达还导致一些其他免疫相关基因表达的改变，包括 Zn72D 的下调。在苍蝇睾丸中敲除 Zn72D 也导致卵孵化率显着降低。这些结果表明，沃尔巴克氏体可能通过免疫相关途径诱导雄性宿主生育能力缺陷，从而导致雄性睾丸氧化损伤和细胞死亡。key 的过度表达还导致一些其他免疫相关基因表达的改变，包括 Zn72D 的下调。在苍蝇睾丸中敲除 Zn72D 也导致卵孵化率显着降低。这些结果表明，沃尔巴克氏体可能通过免疫相关途径诱导雄性宿主生育能力缺陷，从而导致雄性睾丸氧化损伤和细胞死亡。key 的过度表达还导致一些其他免疫相关基因表达的改变，包括 Zn72D 的下调。在苍蝇睾丸中敲除 Zn72D 也导致卵孵化率显着降低。这些结果表明，沃尔巴克氏体可能通过免疫相关途径诱导雄性宿主生育能力缺陷，从而导致雄性睾丸氧化损伤和细胞死亡。