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Ablation of Max expression induces meiotic onset in sexually undifferentiated germ cells

ABSTRACT: MAX (MYC Associated Factor X) is generally known as a mandatory partner for MYC transcription factor, which activates various genes involved in cell growth and metabolism. On the other hand, MAX, when interacting with MGA, forms the polycomb repressive complex (PRC) 1.6, one of the subtypes of PRC1, which directs the transcriptionally repressed chromatin state. Although physiological significance is not known at present, we have previously demonstrated that mouse embryonic stem cells (ESCs) bear a potential to onset meiosis, albeit not germ cells, and PRC1.6 prevent ESCs from their ectopic onset of meiosis (Suzuki et al., 2016, Nat. Commun. 7:11056 doi: 10.1038/ncomms11056). In this study, we aimed to investigate the role of Max in germ cells in vivo by performing the primordial germ cell-specific knockout of the Max gene.

ORGANISM(S): Mus musculus

PROVIDER: GSE233556 | GEO | 2024/03/13

REPOSITORIES: GEO

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MAX controls meiotic entry in sexually undifferentiated germ cells

Project description:In mammals, female, but not male, germ cells onset meiosis physiologically during embryonic stages. We examined whether germ cell-specific disruption of Max gene leads to the activation of meiosis-related genes in embryonic male germ cells by single cell RNA sequencing.

2024-09-29 | GSE244318 | GEO

Pcgf6 suppresses Myc-induced lymphomagenesis [RNA-seq]

Project description:Max is an obligate dimerization partner for the Myc transcription factors and for several repressors, such as Mnt, Mxd1-4 and Mga, collectively thought to antagonize Myc function in transcription and oncogenesis. Mga, in particular, is part of the variant Polycomb group repressive complex PRC1.6. Here, we show that ablation of the distinct PRC1.6 subunit Pcgf6 – but not Mga – accelerates Myc-induced lymphomagenesis in Eµ-myc transgenic mice. Unexpectedly, however, Pcgf6 loss shows no significant impact on transcriptional profiles, in neither pre-tumoral B-cells, nor lymphomas. Altogether, these data unravel an unforeseen, Mga- and PRC1.6-independent tumor suppressor activity of Pcgf6.

2021-12-05 | GSE189999 | GEO

Pcgf6 suppresses Myc-induced lymphomagenesis [ChIP-seq]

2021-12-05 | GSE189989 | GEO

PRC1.6 and SETDB1-mediated repression of germline genes in the early embryo precedes DNA methylation-mediated silencing.

Project description:Silencing of a subset of germline genes is dependent upon DNA methylation (DNAme) post-implantation. However, these genes are generally hypomethylated in the ICM, implicating alternative silencing pathways before implantation. Indeed, in embryonic stem cells (ESCs), an overlapping set of genes, including germline “genome-defence” (GGD) genes, are upregulated following deletion of the H3K9 methyltransferase SETDB1 or subunits of the non-canonical PRC1 complex PRC1.6. Here, we show that in pre-implantation embryos and naïve ESCs (nESCs), hypomethylated promoters of germline genes bound by the PRC1.6 DNA-binding subunits MGA/MAX/E2F6 are enriched for RING1B-dependent H2AK119ub1 and H3K9me3. Accordingly, silencing of these genes in nESCs shows a greater dependence on PRC1.6 than DNAme. In contrast, GGD genes are hypermethylated in epiblast-like cells and their silencing is dependent upon SETDB1, PRC1.6/RING1B and DNAme, with H3K9me3 and DNAme establishment dependent upon MGA binding. Thus, GGD genes are initially repressed by PRC1.6, with DNAme subsequently engaged in post-implantation embryos.

2021-11-05 | GSE171695 | GEO

DNMTs and SETDB1 function as co-repressors in MAX-mediated repression of germ cell-related genes in mouse embryonic stem cells

Project description:In embryonic stem cells (ESCs), the expression of development-related genes, including germ cell-related genes, is globally repressed. The transcription factor MAX represses germ cell-related gene expression in ESCs via PCGF6-polycomb repressive complex (PRC)1, which consists of several epigenetic factors. However, we predicted that MAX represses germ cell-related gene expression through several additional mechanisms because PCGF6-PRC1 regulates the expression of only a subset of genes repressed by MAX. Here, we report that MAX associated with DNA methyltransferases (DNMTs) and the histone methyltransferase SETDB1 cooperatively control germ cell-related gene expression in ESCs. Both DNA methylation and histone H3 lysine 9 tri-methylation of the promoter regions of several germ cell-related genes were not affected by knockout of the PRC1 components, indicating that the MAX-DNMT and MAX-SETDB1 pathways are independent of the PCGF6-PRC1 pathway. Our findings provide insights into our understanding of MAX-based repressive mechanisms of germ cell-related genes in ESCs.

2018-08-31 | GSE102610 | GEO

DNA microarray analysis of G9a knockout embryonic stem cells

Project description:In embryonic stem cells (ESCs), the expression of development-related genes, including germ cell–related genes, is globally repressed. The transcription factor MAX represses germ cell–related gene expression in ESCs via PCGF6-polycomb repressive complex (PRC)1, which consists of several epigenetic factors. However, we predicted that MAX represses germ cell–related gene expression through several additional mechanisms because PCGF6-PRC1 regulates the expression of only a subset of genes repressed by MAX. Here, we report that MAX associated with DNA methyltransferases (DNMTs) and the histone methyltransferase SETDB1 cooperatively control germ cell–related gene expression in ESCs. Both DNA methylation and histone H3 lysine 9 tri-methylation of the promoter regions of several germ cell–related genes were not affected by knockout of the PRC1 components, indicating that the MAX-DNMT and MAX-SETDB1 pathways are independent of the PCGF6-PRC1 pathway. Our findings provide insights into our understanding of MAX-based repressive mechanisms of germ cell–related genes in ESCs.

2018-11-10 | GSE102423 | GEO

Max is a repressor of germ-cell-related gene expression in mouse embryonic stem cells

2013-05-01 | GSE45181 | GEO

Max is a repressor of germ-cell-related gene expression in mouse embryonic stem cells

Project description:Embryonic stem cells (ESCs) and primordial germ cells (PGCs) express many pluripotency-associated genes, but ESCs do not normally undergo conversion into PGCs. Thus, we predicted that there is a mechanism that represses PGC-related gene expression in ESCs. Here we identify genes involved in this putative mechanism, by using an ESC line with a Vasa reporter for an RNAi screen of transcription factor genes expressed in ESCs. We identify 5 genes that result in the expression of Vasa when silenced. Of these, Max is the most striking. Transcriptome analysis reveals that Max knockdown (KD) in ESCs 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 ESCs. In addition, Max-KD results in a decrease in histone H3K9 dimethylation at their promoter regions. We propose that Max is part of a protein complex that acts as a repressor of germ-cell-related genes in ESCs. Gene expression profile of Vasa-positive cells isolated from Max knockdown ESCs was compared to that of normal ESCs and in vivo PGCs. As an ESCs sample, a mouse embryonic stem cell line that carries a Venus reporter driven by the Vasa gene promoter (VV3) was used for this study. VV3 ESCs were transfected with non-silencing negative control siRNA (AllStars) or siRNA against the Max gene. Vasa-positive cells were purified using fluorescence-activated cell sorting (FACS). As a PGCs sample, a mouse strain that carries a germ-cell-specific GFP reporter (Oct4M-NM-^TPE-GFP) was used. PGCs were also purified using FACS. RNA samples were isolated from each sample and labeled and hybridized to Agilent microarrays. Three biological replicates were performed for each group of samples.

2013-05-01 | E-GEOD-45181 | biostudies-arrayexpress

Effect of ablation of Max gene expression on ES cells cultured under conventional or 2i/Nam condition.

2011-07-20 | GSE27881 | GEO

Effect of ablation of Max gene expression on ES cells cultured under conventional or 2i/Nam condition.

Project description:c-Myc is one of key players that are crucially involved in maintaining the undifferentiated state and the self-renewal of ESCs. To understand the mechanism by which c-Myc helps preserve these prominent characteristics of ESCs, we generated null-ES cells for the Max gene, which encodes the best characterized partner protein for all Myc family proteins. Although Myc/Max complexes have been widely regarded as crucial regulators of the ESC status, our data reveal that ESCs do not absolutely require these complexes in so-called ground state or related conditons and that this requirement is restricted to conventional ES culture conditions without using a MAPK inhibitor. Simply Dox-treated or Nanog (WT or D67G mutant)-rescued Max-null ESCs which were cultured under conventional culture condition and 2i/Nam-treated completely Max-null ES cells from which Dox-regulatable cDNA was removed were used for RNA source. Samples from Dox-untreated Max-null ESCs cultured under conventional culture condition were used as reference samples for Dox-treated cells and Nanog-rescued cells, while a sample from wild-type ESCs cultured under 2i/Nam condition was used as a reference sample for completely Max-null ES cells cultured with 2i/Nam.

2011-07-19 | E-GEOD-27881 | biostudies-arrayexpress

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