State Key Laboratory of Molecular Biology, Shanghai Key Laboratory of Molecular Andrology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
State Key Laboratory of Reproductive Medicine and Offspring Health, Jiangsu Laboratory Animal Center, Jiangsu Animal Experimental Center of Medicine and Pharmacy, Department of Cell Biology, Animal Core facility, Key Laboratory of Model Animal, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, 211166, China.
Nat Commun. 2023 Aug 29;14(1):5267. doi: 10.1038/s41467-023-40650-x.
The piRNA pathway is essential for female fertility in golden hamsters and likely humans, but not in mice. However, the role of individual PIWIs in mammalian reproduction remains poorly understood outside of mice. Here, we describe the expression profiles, subcellular localization, and knockout-associated reproductive defects for all four PIWIs in golden hamsters. In female golden hamsters, PIWIL1 and PIWIL3 are highly expressed throughout oogenesis and early embryogenesis, while knockout of PIWIL1 leads to sterility, and PIWIL3 deficiency results in subfertility with lagging zygotic development. PIWIL1 can partially compensate for TE silencing in PIWIL3 knockout females, but not vice versa. PIWIL1 and PIWIL4 are the predominant PIWIs expressed in adult and postnatal testes, respectively, while PIWIL2 is present at both stages. Loss of any PIWI expressed in testes leads to sterility and severe but distinct spermatogenesis disorders. These findings illustrate the non-redundant regulatory functions of PIWI-piRNAs in gametogenesis and early embryogenesis in golden hamsters, facilitating study of their role in human fertility.
piRNA 通路对于金黄仓鼠和可能的人类的雌性生育能力至关重要，但对于小鼠则不然。然而，除了小鼠之外，个体 PIWI 在哺乳动物生殖中的作用仍然知之甚少。在这里，我们描述了金黄仓鼠中所有四个 PIWIs 的表达谱、亚细胞定位以及敲除相关的生殖缺陷。在雌性金黄仓鼠中，PIWIL1 和 PIWIL3 在整个卵子发生和早期胚胎发生过程中高度表达，而 PIWIL1 的敲除导致不育，而 PIWIL3 的缺乏导致胚胎发育滞后的亚不育。PIWIL1 可以部分补偿 PIWIL3 敲除雌性中的 TE 沉默，但反之则不行。PIWIL1 和 PIWIL4 分别是成年和出生后睾丸中表达最丰富的 PIWI，而 PIWIL2 则存在于两个阶段。任何在睾丸中表达的 PIWI 的缺失都会导致不育和严重但不同的精子发生障碍。这些发现说明了 PIWI-piRNAs 在金黄仓鼠配子发生和早期胚胎发生中的非冗余调节功能，有助于研究它们在人类生育能力中的作用。
