Loss of MAX results in meiotic entry in mouse embryonic and germline stem cells

Ayumu Suzuki, Masataka Hirasaki, Tomoaki Hishida, Jun Wu, Daiji Okamura, Atsushi Ueda, Masazumi Nishimoto, Yutaka Nakachi, Yosuke Mizuno, Yasushi Okazaki, Yasuhisa Matsui, Juan Carlos Izpisua Belmonte () and Akihiko Okuda ()
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Ayumu Suzuki: Research Center for Genomic Medicine, Saitama Medical University
Masataka Hirasaki: Research Center for Genomic Medicine, Saitama Medical University
Tomoaki Hishida: Research Center for Genomic Medicine, Saitama Medical University
Jun Wu: Gene Expression Laboratory, Salk Institute for Biological Studies
Daiji Okamura: Gene Expression Laboratory, Salk Institute for Biological Studies
Atsushi Ueda: Research Center for Genomic Medicine, Saitama Medical University
Masazumi Nishimoto: Research Center for Genomic Medicine, Saitama Medical University
Yutaka Nakachi: Research Center for Genomic Medicine, Saitama Medical University
Yosuke Mizuno: Research Center for Genomic Medicine, Saitama Medical University
Yasushi Okazaki: Research Center for Genomic Medicine, Saitama Medical University
Yasuhisa Matsui: Cell Resource Center for Biomedical Research, Institute of Development, Aging and Cancer, Tohoku University
Juan Carlos Izpisua Belmonte: Gene Expression Laboratory, Salk Institute for Biological Studies
Akihiko Okuda: Research Center for Genomic Medicine, Saitama Medical University

Nature Communications, 2016, vol. 7, issue 1, 1-15

Abstract: Abstract Meiosis is a unique process that allows the generation of reproductive cells. It remains largely unknown how meiosis is initiated in germ cells and why non-germline cells do not undergo meiosis. We previously demonstrated that knockdown of Max expression, a gene encoding a partner of MYC family proteins, strongly activates expression of germ cell-related genes in ESCs. Here we find that complete ablation of Max expression in ESCs results in profound cytological changes reminiscent of cells undergoing meiotic cell division. Furthermore, our analyses uncovers that Max expression is transiently attenuated in germ cells undergoing meiosis in vivo and its forced reduction induces meiosis-like cytological changes in cultured germline stem cells. Mechanistically, Max depletion alterations are, in part, due to impairment of the function of an atypical PRC1 complex (PRC1.6), in which MAX is one of the components. Our data highlight MAX as a new regulator of meiotic onset.

Date: 2016
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DOI: 10.1038/ncomms11056

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