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LSD1 is essential for oocyte meiotic progression by regulating CDC25B expression in mice

Author

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  • Jeesun Kim

    (The University of Texas MD Anderson Cancer Center, Science Park
    Center for Cancer Epigenetics, The University of Texas MD Anderson Cancer Center, Science Park)

  • Anup Kumar Singh

    (The University of Texas MD Anderson Cancer Center, Science Park
    Center for Cancer Epigenetics, The University of Texas MD Anderson Cancer Center, Science Park)

  • Yoko Takata

    (The University of Texas MD Anderson Cancer Center, Science Park)

  • Kevin Lin

    (The University of Texas MD Anderson Cancer Center, Science Park)

  • Jianjun Shen

    (The University of Texas MD Anderson Cancer Center, Science Park)

  • Yue Lu

    (The University of Texas MD Anderson Cancer Center, Science Park
    Center for Cancer Epigenetics, The University of Texas MD Anderson Cancer Center, Science Park)

  • Marc A. Kerenyi

    (Boston Children’s Hospital and Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Harvard Medical School)

  • Stuart H. Orkin

    (Boston Children’s Hospital and Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Harvard Medical School
    Howard Hughes Medical Institute, Harvard Medical School)

  • Taiping Chen

    (The University of Texas MD Anderson Cancer Center, Science Park
    Center for Cancer Epigenetics, The University of Texas MD Anderson Cancer Center, Science Park)

Abstract

Mammalian oocytes are arrested at prophase I until puberty when hormonal signals induce the resumption of meiosis I and progression to meiosis II. Meiotic progression is controlled by CDK1 activity and is accompanied by dynamic epigenetic changes. Although the signalling pathways regulating CDK1 activity are well defined, the functional significance of epigenetic changes remains largely unknown. Here we show that LSD1, a lysine demethylase, regulates histone H3 lysine 4 di-methylation (H3K4me2) in mouse oocytes and is essential for meiotic progression. Conditional deletion of Lsd1 in growing oocytes results in precocious resumption of meiosis and spindle and chromosomal abnormalities. Consequently, most Lsd1-null oocytes fail to complete meiosis I and undergo apoptosis. Mechanistically, upregulation of CDC25B, a phosphatase that activates CDK1, is responsible for precocious meiotic resumption and also contributes to subsequent spindle and chromosomal defects. Our findings uncover a functional link between LSD1 and the major signalling pathway governing meiotic progression.

Suggested Citation

  • Jeesun Kim & Anup Kumar Singh & Yoko Takata & Kevin Lin & Jianjun Shen & Yue Lu & Marc A. Kerenyi & Stuart H. Orkin & Taiping Chen, 2015. "LSD1 is essential for oocyte meiotic progression by regulating CDC25B expression in mice," Nature Communications, Nature, vol. 6(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms10116
    DOI: 10.1038/ncomms10116
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    Cited by:

    1. Long Bai & Yu Xiang & Minyue Tang & Shuangying Liu & Qingqing Chen & Qichao Chen & Min Zhang & Shan Wan & Yimiao Sang & Qingfang Li & Sisi Wang & Zhekun Li & Yang Song & Xiaoling Hu & Luna Mao & Guofa, 2023. "ALKBH5 controls the meiosis-coupled mRNA clearance in oocytes by removing the N 6-methyladenosine methylation," Nature Communications, Nature, vol. 14(1), pages 1-21, December.
    2. Zhuo Han & Rui Wang & Pengliang Chi & Zihan Zhang & Ling Min & Haizhan Jiao & Guojin Ou & Dan Zhou & Dandan Qin & Chengpeng Xu & Zheng Gao & Qianqian Qi & Jialu Li & Yuechao Lu & Xiang Wang & Jing Che, 2024. "The subcortical maternal complex modulates the cell cycle during early mammalian embryogenesis via 14-3-3," Nature Communications, Nature, vol. 15(1), pages 1-18, December.

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