ArticleNature communications2016
Loss of MAX results in meiotic entry in mouse embryonic and germline stem cells.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 80 citations in OpenAlex.
- Conserved signaling pathways and transcriptional regulators drive ovarian aging across species.Poultry science · 2026Article
- Molecular genetics of meiotic initiation in mammals.Biology of reproduction · 2026Article
- MCT1 governs a metabolic checkpoint at pachytene during spermatogenesis.Research square · 2026Article
- MCT1 governs a metabolic checkpoint at pachytene during spermatogenesis.bioRxiv : the preprint server for biology · 2026Article
- Epigenetic relay: Polycomb-directed DNA methylation in mammalian development.PLoS genetics · 2025Review
- MGA directly recruits SETDB1/ATF7IP for histone H3K9me3 mark on meiosis-related genes in mouse embryonic stem cells.iScience · 2025Article
- Initiation of meiosis from human iPSCs under defined conditions through identification of regulatory factors.Science advances · 2025Article
- KDM5C is a sex-biased brake against germline gene expression programs in somatic lineages.bioRxiv : the preprint server for biology · 2024Article
- Destabilization of mRNAs enhances competence to initiate meiosis in mouse spermatogenic cells.Development (Cambridge, England) · 2024Article
- Epigenetic priming in the male germline.Current opinion in genetics & development · 2024Review
- Induction of Meiosis from Human Pluripotent Stem Cells.bioRxiv : the preprint server for biology · 2024Article
- MAX controls meiotic entry in sexually undifferentiated germ cells.Scientific reports · 2024Article
- Epigenetic programming in the ovarian reserve.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Article
- Systematic identification of factors involved in the silencing of germline genes in mouse embryonic stem cells.Nucleic acids research · 2023Article
- PFOA-Induced Ovotoxicity Differs Between Lean and Obese Mice With Impacts on Ovarian Reproductive and DNA Damage Sensing and Repair Proteins.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- The Beginning of Meiosis in Mammalian Female Germ Cells: A Never-Ending Story of Intrinsic and Extrinsic Factors.International journal of molecular sciences · 2022Review
- Review
- Rif1 interacts with non-canonical polycomb repressive complex PRC1.6 to regulate mouse embryonic stem cells fate potential.Cell regeneration (London, England) · 2022Article
- DNA binding by polycomb-group proteins: searching for the link to CpG islands.Nucleic acids research · 2022Review
- Soma-to-germline transformation in chromatin-linked neurodevelopmental disorders?The FEBS journal · 2022Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.