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

Jeesun Kim, Anup Kumar Singh, Yoko Takata, Kevin Lin, Jianjun Shen, Yue Lu, Marc A. Kerenyi, Stuart H. Orkin and Taiping Chen ()
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Jeesun Kim: The University of Texas MD Anderson Cancer Center, Science Park
Anup Kumar Singh: 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
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
Taiping Chen: The University of Texas MD Anderson Cancer Center, Science Park

Nature Communications, 2015, vol. 6, issue 1, 1-14

Abstract: 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.

Date: 2015
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DOI: 10.1038/ncomms10116

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