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Nat Commun. 2016 Mar 30;7:11056. doi: 10.1038/ncomms11056.

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

Author information

1
Division of Developmental Biology, Research Center for Genomic Medicine, Saitama Medical University, Yamane Hidaka, Saitama 350-1241, Japan.
2
Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.
3
Universidad Católica San Antonio de Murcia (UCAM) Campus de los Jerónimos, No. 135, Guadalupe, 30107 Murcia, Spain.
4
Division of Translational Research, Research Center for Genomic Medicine, Saitama Medical University, Yamane Hidaka, Saitama 350-1241, Japan.
5
Division of Functional Genomics and Systems Medicine, Research Center for Genomic Medicine, Saitama Medical University, Yamane Hidaka, Saitama 350-1241, Japan.
6
Cell Resource Center for Biomedical Research, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan.
7
Japan Agency for Medical Research and Development and Development-Core Research for Evolutionary Science and Technology (AMED-CREST), Tokyo 100-0004, Japan.

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.

PMID:
27025988
PMCID:
PMC4820925
DOI:
10.1038/ncomms11056
[Indexed for MEDLINE]
Free PMC Article

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