ArticleNature communications2013
Max is a repressor of germ cell-related gene expression in mouse embryonic stem cells.
Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 75 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
- 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
- Destabilization of mRNAs enhances competence to initiate meiosis in mouse spermatogenic cells.Development (Cambridge, England) · 2024Article
- MAX controls meiotic entry in sexually undifferentiated germ cells.Scientific reports · 2024Article
- A functional crosstalk between the H3K9 methylation writers and their reader HP1 in safeguarding embryonic stem cell identity.Stem cell reports · 2023Article
- Unreprogrammed H3K9me3 prevents minor zygotic genome activation and lineage commitment in SCNT embryos.Nature communications · 2023Article
- Systematic identification of factors involved in the silencing of germline genes in mouse embryonic stem cells.Nucleic acids research · 2023Article
- Epigenetic markers in the embryonal germ cell development and spermatogenesis.Basic and clinical andrology · 2023Review
- Review
- Rif1 interacts with non-canonical polycomb repressive complex PRC1.6 to regulate mouse embryonic stem cells fate potential.Cell regeneration (London, England) · 2022Article
- Soma-to-germline transformation in chromatin-linked neurodevelopmental disorders?The FEBS journal · 2022Review
- Article
- Contribution ofFrontiers in cell and developmental biology · 2022Article
- p53 inactivation unmasks histone methylation-independent WDR5 functions that drive self-renewal and differentiation of pluripotent stem cells.Stem cell reports · 2021Article
- Loss of MGA repression mediated by an atypical polycomb complex promotes tumor progression and invasiveness.eLife · 2021Article
- E2F6 initiates stable epigenetic silencing of germline genes during embryonic development.Nature communications · 2021Article
- Mga safeguards embryonic stem cells from acquiring extraembryonic endoderm fates.Science advances · 2021Article
- The fibronectin type-III (FNIII) domain of ATF7IP contributes to efficient transcriptional silencing mediated by the SETDB1 complex.Epigenetics & chromatin · 2020Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Embryonic stem cells and primordial germ cells (PGCs) express many pluripotency-associated genes, but embryonic stem cells do not normally undergo conversion into primordial germ cells. Thus, we predicted that there is a mechanism that represses primordial germ cell-related gene expression in embryonic stem cells. Here we identify genes involved in this putative mechanism, by using an embryonic stem cell line with a Vasa reporter in an RNA interference screen of transcription factor genes expressed in embryonic stem cells. We identify five genes that result in the expression of Vasa when silenced. Of these, Max is the most striking. Transcriptome analysis reveals that Max knockdown in embryonic stem cells results in selective, global derepression of germ cell-specific genes. Max interacts with histone H3K9 methyltransferases and associates with the germ cell-specific genes in embryonic stem cells. In addition, Max knockdown results in a decrease in histone H3K9 dimethylation at their promoter regions. We propose that Max is part of protein complex that acts as a repressor of germ cell-related genes in embryonic stem cells.
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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.