Many animals have a conserved adaptive genome defence system known as the Piwi-interacting RNA (piRNA) pathway, which is essential for germ cell development and function. Disruption of individual mouse Piwi genes results in male but not female sterility, leading to the assumption that PIWI genes play little or no role in mammalian oocytes. Here, we report the generation of PIWI-defective golden hamsters, which have defects in the production of functional oocytes. The mechanisms involved vary among the hamster PIWI genes, whereby the lack of PIWIL1 has a major impact on gene expression, including hamster-specific young transposon de-silencing, whereas PIWIL3 deficiency has little impact on gene expression in oocytes, although DNA methylation was reduced to some extent in PIWIL3-deficient oocytes. Our findings serve as the foundation for developing useful models to study the piRNA pathway in mammalian oocytes, including humans.

许多动物都有一个保守的适应性基因组防御系统，称为 Piwi 相互作用 RNA (piRNA) 途径，这对于生殖细胞的发育和功能至关重要。单个小鼠 Piwi 基因的破坏导致雄性而不是雌性不育，导致假设 PIWI 基因在哺乳动物卵母细胞中几乎没有作用或没有作用。在这里，我们报告了 PIWI 缺陷金仓鼠的产生，它们在功能性卵母细胞的产生方面存在缺陷。涉及的机制因仓鼠 PIWI 基因而异，其中PIWIL1的缺乏对基因表达有重大影响，包括仓鼠特异性年轻转座子去沉默，而PIWIL3缺乏对卵母细胞中的基因表达影响不大，尽管 DNA 甲基化降低在某种程度上在PIWIL3 缺陷型卵母细胞。我们的研究结果为开发有用的模型来研究哺乳动物卵母细胞（包括人类）中的 piRNA 途径奠定了基础。