In many animals, germline development is initiated by proteins and RNAs that are expressed maternally. PIWI proteins and their associated small noncoding PIWI-interacting RNAs (piRNAs), which guide PIWI to target RNAs by base-pairing, are among the maternal components deposited into the germline of the Drosophila early embryo. Piwi has been extensively studied in the adult ovary and testis, where it is required for transposon suppression, germline stem cell self-renewal, and fertility. Consequently, loss of Piwi in the adult ovary using piwi-null alleles or knockdown from early oogenesis results in complete sterility, limiting investigation into possible embryonic functions of maternal Piwi. In this study, we show that the maternal Piwi protein persists in the embryonic germline through gonad coalescence, suggesting that maternal Piwi can regulate germline development beyond early embryogenesis. Using a maternal knockdown strategy, we find that maternal Piwi is required for the fertility and normal gonad morphology of female, but not male, progeny. Following maternal piwi knockdown, transposons were mildly derepressed in the early embryo but were fully repressed in the ovaries of adult progeny. Furthermore, the maternal piRNA pool was diminished, reducing the capacity of the PIWI/piRNA complex to target zygotic genes during embryogenesis. Examination of embryonic germ cell proliferation and ovarian gene expression showed that the germline of female progeny was partially masculinized by maternal piwi knockdown. Our study reveals a novel role for maternal Piwi in the germline development of female progeny and suggests that the PIWI/piRNA pathway is involved in germline sex determination in Drosophila.

中文翻译：

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母体 Piwi 调节原始生殖细胞发育以确保果蝇雌性后代的生育能力。

在许多动物中，生殖系发育是由母体表达的蛋白质和 RNA 启动的。PIWI 蛋白及其相关的小型非编码 PIWI 相互作用 RNA (piRNA)，它们通过碱基配对引导 PIWI 靶向 RNA，是沉积在果蝇早期胚胎生殖系中的母体成分之一。Piwi 已在成人卵巢和睾丸中进行了广泛的研究，在那里它是转座子抑制、生殖系干细胞自我更新和生育能力所必需的。因此，使用 piwi-null 等位基因或早期卵子发生敲除导致成年卵巢中 Piwi 的丧失导致完全不育，从而限制了对母体 Piwi 可能的胚胎功能的研究。在这项研究中，我们表明母体 Piwi 蛋白通过性腺合并持续存在于胚胎生殖系中，表明母体 Piwi 可以在早期胚胎发生之外调节生殖系发育。使用母体击倒策略，我们发现母体 Piwi 是女性后代的生育能力和正常性腺形态所必需的，但不是男性后代。在母体 piwi 敲低后，转座子在早期胚胎中被轻度抑制，但在成年后代的卵巢中被完全抑制。此外，母体 piRNA 库减少，降低了 PIWI/piRNA 复合物在胚胎发生过程中靶向合子基因的能力。胚胎生殖细胞增殖和卵巢基因表达的检查表明，雌性后代的生殖系被母体 piwi 敲低部分男性化。