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hnRNPH1 recruits PTBP2 and SRSF3 to modulate alternative splicing in germ cells

Author

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  • Shenglei Feng

    (Huazhong University of Science and Technology)

  • Jinmei Li

    (Huazhong University of Science and Technology)

  • Hui Wen

    (Huazhong University of Science and Technology)

  • Kuan Liu

    (Huazhong University of Science and Technology)

  • Yiqian Gui

    (Huazhong University of Science and Technology)

  • Yujiao Wen

    (Huazhong University of Science and Technology)

  • Xiaoli Wang

    (Huazhong University of Science and Technology)

  • Shuiqiao Yuan

    (Huazhong University of Science and Technology
    Huazhong University of Science and Technology
    Shenzhen Huazhong University of Science and Technology Research Institute)

Abstract

Coordinated regulation of alternative pre-mRNA splicing is essential for germ cell development. However, the underlying molecular mechanism that controls alternative mRNA expression during germ cell development remains elusive. Herein, we show that hnRNPH1 is highly expressed in the reproductive system and recruits the PTBP2 and SRSF3 to modulate the alternative splicing in germ cells. Conditional knockout Hnrnph1 in spermatogenic cells causes many abnormal splicing events, thus affecting the genes related to meiosis and communication between germ cells and Sertoli cells. This is characterized by asynapsis of chromosomes and impairment of germ-Sertoli communications, which ultimately leads to male sterility. Markedly, Hnrnph1 germline-specific mutant female mice are also infertile, and Hnrnph1-deficient oocytes exhibit a similar defective synapsis and cell-cell junction as seen in Hnrnph1-deficient male germ cells. Collectively, our data support a molecular model wherein hnRNPH1 governs a network of alternative splicing events in germ cells via recruitment of PTBP2 and SRSF3.

Suggested Citation

  • Shenglei Feng & Jinmei Li & Hui Wen & Kuan Liu & Yiqian Gui & Yujiao Wen & Xiaoli Wang & Shuiqiao Yuan, 2022. "hnRNPH1 recruits PTBP2 and SRSF3 to modulate alternative splicing in germ cells," Nature Communications, Nature, vol. 13(1), pages 1-19, December.
    • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-31364-7
    DOI: 10.1038/s41467-022-31364-7
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    1. Juan Dong & Xiaoli Wang & Congcong Cao & Yujiao Wen & Akihiko Sakashita & Si Chen & Jin Zhang & Yue Zhang & Liquan Zhou & Mengcheng Luo & Mingxi Liu & Aihua Liao & Satoshi H. Namekawa & Shuiqiao Yuan, 2019. "UHRF1 suppresses retrotransposons and cooperates with PRMT5 and PIWI proteins in male germ cells," Nature Communications, Nature, vol. 10(1), pages 1-14, December.
    2. Wenbo Liu & Fengchao Wang & Qianhua Xu & Junchao Shi & Xiaoxin Zhang & Xukun Lu & Zhen-Ao Zhao & Zheng Gao & Huaixiao Ma & Enkui Duan & Fei Gao & Shaorong Gao & Zhaohong Yi & Lei Li, 2017. "BCAS2 is involved in alternative mRNA splicing in spermatogonia and the transition to meiosis," Nature Communications, Nature, vol. 8(1), pages 1-11, April.
    3. Timothy W. Nilsen & Brenton R. Graveley, 2010. "Expansion of the eukaryotic proteome by alternative splicing," Nature, Nature, vol. 463(7280), pages 457-463, January.
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