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异质性核糖核蛋白H1(hnRNPH1)通过与多聚嘧啶结合蛋白1(PTBP1)和雄激素受体(AR)合作建立支持细胞-生殖细胞间的串扰,对小鼠雄性生育力至关重要。

hnRNPH1 establishes Sertoli-germ cell crosstalk through cooperation with PTBP1 and AR, and is essential for male fertility in mice.

作者信息

Feng Shenglei, Wen Hui, Liu Kuan, Xiong Mengneng, Li Jinmei, Gui Yiqian, Lv Chunyu, Zhang Jin, Ma Xixiang, Wang Xiaoli, Yuan Shuiqiao

机构信息

Institute of Reproductive Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

Laboratory of Animal Center, Huazhong University of Science and Technology, Wuhan 430030, China.

出版信息

Development. 2023 Feb 15;150(3). doi: 10.1242/dev.201040. Epub 2023 Jan 31.

Abstract

Spermatogenesis depends on the crosstalk of Sertoli cells (SCs) and germ cells. However, the gene regulatory network establishing the communications between SCs and germ cells remains unclear. Here, we report that heterogeneous nuclear ribonucleoprotein H1 (hnRNPH1) in SCs is essential for the establishment of crosstalk between SCs and germ cells. Conditional knockout of hnRNPH1 in mouse SCs leads to compromised blood-testis barrier function, delayed meiotic progression, increased germ cell apoptosis, sloughing of germ cells and, eventually, infertility of mice. Mechanistically, we discovered that hnRNPH1 could interact with the splicing regulator PTBP1 in SCs to regulate the pre-mRNA alternative splicing of the target genes functionally related to cell adhesion. Interestingly, we also found hnRNPH1 could cooperate with the androgen receptor, one of the SC-specific transcription factors, to modulate the transcription level of a group of genes associated with the cell-cell junction and EGFR pathway by directly binding to the gene promoters. Collectively, our findings reveal a crucial role for hnRNPH1 in SCs during spermatogenesis and uncover a potential molecular regulatory network involving hnRNPH1 in establishing Sertoli-germ cell crosstalk.

摘要

精子发生依赖于支持细胞(SCs)与生殖细胞之间的相互作用。然而,建立支持细胞与生殖细胞间通讯的基因调控网络仍不清楚。在此,我们报道支持细胞中的异质性核糖核蛋白H1(hnRNPH1)对于支持细胞与生殖细胞间相互作用的建立至关重要。在小鼠支持细胞中条件性敲除hnRNPH1会导致血睾屏障功能受损、减数分裂进程延迟、生殖细胞凋亡增加、生殖细胞脱落,最终导致小鼠不育。机制上,我们发现hnRNPH1可与支持细胞中的剪接调节因子PTBP1相互作用,以调控与细胞黏附功能相关的靶基因的前体mRNA可变剪接。有趣的是,我们还发现hnRNPH1可与支持细胞特异性转录因子之一雄激素受体协同作用,通过直接结合基因启动子来调节一组与细胞间连接和表皮生长因子受体(EGFR)途径相关基因的转录水平。总的来说,我们的研究结果揭示了hnRNPH1在精子发生过程中支持细胞中的关键作用,并揭示了一个涉及hnRNPH1建立支持细胞-生殖细胞相互作用的潜在分子调控网络。

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