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

Author

Listed:
  • 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
    Gene Expression Laboratory, Salk Institute for Biological Studies)

  • Jun Wu

    (Gene Expression Laboratory, Salk Institute for Biological Studies)

  • Daiji Okamura

    (Gene Expression Laboratory, Salk Institute for Biological Studies
    Universidad Católica San Antonio de Murcia (UCAM))

  • 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
    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
    Research Center for Genomic Medicine, Saitama Medical University)

  • Yasuhisa Matsui

    (Cell Resource Center for Biomedical Research, Institute of Development, Aging and Cancer, Tohoku University
    Japan Agency for Medical Research and Development and Development-Core Research for Evolutionary Science and Technology (AMED-CREST))

  • Juan Carlos Izpisua Belmonte

    (Gene Expression Laboratory, Salk Institute for Biological Studies)

  • Akihiko Okuda

    (Research Center for Genomic Medicine, Saitama Medical University)

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.

Suggested Citation

  • Ayumu Suzuki & Masataka Hirasaki & Tomoaki Hishida & Jun Wu & Daiji Okamura & Atsushi Ueda & Masazumi Nishimoto & Yutaka Nakachi & Yosuke Mizuno & Yasushi Okazaki & Yasuhisa Matsui & Juan Carlos Izpis, 2016. "Loss of MAX results in meiotic entry in mouse embryonic and germline stem cells," Nature Communications, Nature, vol. 7(1), pages 1-15, April.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11056
    DOI: 10.1038/ncomms11056
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    Cited by:

    1. Kentaro Mochizuki & Jafar Sharif & Kenjiro Shirane & Kousuke Uranishi & Aaron B. Bogutz & Sanne M. Janssen & Ayumu Suzuki & Akihiko Okuda & Haruhiko Koseki & Matthew C. Lorincz, 2021. "Repression of germline genes by PRC1.6 and SETDB1 in the early embryo precedes DNA methylation-mediated silencing," Nature Communications, Nature, vol. 12(1), pages 1-15, December.

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