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Polycomb-mediated axial patterning requires nucleosome compaction [ChIP-seq]

ABSTRACT: We determined the genome-wide binding profiles of wild type and compaction mutant CBX2 (denoted as 'KRA') in mouse embryonic stem cells (mESCs) by ChIP-seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE86084 | GEO | 2017/08/31

SECONDARY ACCESSION(S): PRJNA340228

REPOSITORIES: GEO

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Polycomb-mediated axial patterning requires nucleosome compaction [RNA-seq]

Project description:We determined by RNA-seq gene expression changes in mESCs following the induced expression of WT-, KRA- or DEA-CBX2 variants in Cbx2 null cells.

2017-08-31 | GSE86083 | GEO

Polycomb-mediated axial patterning requires nucleosome compaction

Project description:Polycomb-mediated axial patterning requires nucleosome compaction

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Polycomb-mediated axial patterning requires nucleosome compaction

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-08-31 | GSE86085 | GEO

Mutation of a nucleosome compaction region disrupts Polycomb-mediated axial patterning.

Project description:Nucleosomes play important structural and regulatory roles by tightly wrapping the DNA that constitutes the metazoan genome. The Polycomb group (PcG) proteins modulate nucleosomes to maintain repression of key developmental genes, including Hox genes whose temporal and spatial expression is tightly regulated to guide patterning of the anterior-posterior body axis. CBX2, a component of the mammalian Polycomb repressive complex 1 (PRC1), contains a compaction region that has the biochemically defined activity of bridging adjacent nucleosomes. Here, we demonstrate that a functional compaction region is necessary for proper body patterning, because mutating this region leads to homeotic transformations similar to those observed with PcG loss-of-function mutations. We propose that CBX2-driven nucleosome compaction is a key mechanism by which PcG proteins maintain gene silencing during mouse development.

| S-EPMC5503153 | biostudies-literature

Polycomb-mediated chromatin compaction during cell differentiation

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Compaction of chromatin by diverse Polycomb group proteins requires localized regions of high charge.

Project description:Polycomb group (PcG) proteins are required for the epigenetic maintenance of developmental genes in a silent state. Proteins in the Polycomb-repressive complex 1 (PRC1) class of the PcG are conserved from flies to humans and inhibit transcription. One hypothesis for PRC1 mechanism is that it compacts chromatin, based in part on electron microscopy experiments demonstrating that Drosophila PRC1 compacts nucleosomal arrays. We show that this function is conserved between Drosophila and mouse PRC1 complexes and requires a region with an overrepresentation of basic amino acids. While the active region is found in the Posterior Sex Combs (PSC) subunit in Drosophila, it is unexpectedly found in a different PRC1 subunit, a Polycomb homolog called M33, in mice. We provide experimental support for the general importance of a charged region by predicting the compacting capability of PcG proteins from species other than Drosophila and mice and by testing several of these proteins using solution assays and microscopy. We infer that the ability of PcG proteins to compact chromatin in vitro can be predicted by the presence of domains of high positive charge and that PRC1 components from a variety of species conserve this highly charged region. This supports the hypothesis that compaction is a key aspect of PcG function.

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Caenorhabditis elegans embryonic axial patterning requires two recently discovered posterior-group Hox genes.

Project description:Hox genes encode highly conserved transcription factors that control regional identities of cells and tissues along the developing anterior-posterior axis, probably in all bilaterian metazoans. However, in invertebrate embryos other than Drosophila, Hox gene functions remain largely unknown except by inference from sequence similarities and expression patterns. Recent genomic sequencing has shown that Caenorhabditis elegans has three Hox genes of the posterior paralog group [Ruvkun, G. & Hobert, O. (1998) Science 282, 2033-2041]. However, only one has been previously identified genetically, and it is not required for embryonic development [Chisholm, A. (1991) Development (Cambridge, U.K.) 111, 921-932]. Herein, we report identification of the remaining two posterior paralogs as the nob-1 gene and the neighboring php-3 gene. Elimination of nob-1 and php-3 functions causes gross embryonic defects in both posterior patterning and morphogenetic movements of the posterior hypodermis, as well as posterior-to-anterior cell fate transformations and lethality. The only other Hox gene essential for embryogenesis is the labial/Hox1 homolog ceh-13, required for more anterior patterning [Brunschwig, K., Wittmann, C., Schnabel, R., Burglin, T. R., Tobler, H. & Muller, F. (1999) Development (Cambridge, U.K.) 126, 1537-1546]. Therefore, essential embryonic patterning in C. elegans requires only Hox genes of the anterior and posterior paralog groups, raising interesting questions about evolution of the medial-group genes.

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Dual function of H2AK119ub1 on gene regulation via modulating canonical-PRC1 and H1-dependent chromatin compaction H2AK119ub1 deferentially fine-tunes gene expression by modulating canonical-PRC1 and H1-dependent chromatin compaction

Project description:First, we applied ChIP-seq (Chromatin Immunoprecipitation) to measure the enrichment of Cbx7, Ring1B, and H3K27me3 on DNA in WT (wild-type), Ring1bI53A, and Rybp/Yaf2-DKO ESCs. The results suggest that accumulation of cPRC1 on chromatin isn’t caused by the mis-regulation of H3K27me3 in Ring1bI53A mESCs and Rybp/Yaf2-DKO impairs the accumulation of ncPRC1 on chromatin. Next, here we adopt ChIP-seq to investigate the dynamic of Ring1B and Cbx7 on DNA during Rybp/Yaf2 degradation after IAA treatment. We found that that H2AK119ub1 plays an important role in restricting the binding of cPRC1 on chromatin and thereby compromises cPRC1-mediated chromatin compaction. And then, we carried out mRNA-seq and identified differential expressed genes among WT and Ring1bI53A mESCs. Next, we applied ChIP-seq (Chromatin Immunoprecipitation) to measure the enrichment of Cbx7, Ring1B, Jarid2, PHC1, and PCGF2 on DNA in WT (wild-type), Ring1bI53A, and Bap1-KO ESCs . The results suggest that the binding of “all cPRC1” with nucleosomes is blocked by H2AK119ub1. Finally, here we performed MNase-seq in WT and H1-QKO mESCs. We found that H1-QKO lead to a stronger decondensation of H2Aub1_enriched TSSs compared with residual TSS regions. The result of ChIP-seq for H1 and ATAC-seq (Assay for Transposase Accessible Chromatin with high-throughput sequencing) of WT and Ring1BI53A, and mRNA-seq of WT and H1-QKO mESCs suggest H2AK119ub1 represses genes via promoting H1-mediated chromatin compaction.

2024-02-11 | GSE232140 | GEO

Lin28a/let-7 pathway modulates the Hox code via Polycomb regulation during axial patterning in vertebrates.

Project description:The body plan along the anteroposterior axis and regional identities are specified by the spatiotemporal expression of Hox genes. Multistep controls are required for their unique expression patterns; however, the molecular mechanisms behind the tight control of Hox genes are not fully understood. In this study, we demonstrated that the Lin28a/let-7 pathway is critical for axial elongation. Lin28a-/- mice exhibited axial shortening with mild skeletal transformations of vertebrae, which were consistent with results in mice with tail bud-specific mutants of Lin28a. The accumulation of let-7 in Lin28a-/- mice resulted in the reduction of PRC1 occupancy at the Hox cluster loci by targeting Cbx2. Consistently, Lin28a loss in embryonic stem-like cells led to aberrant induction of posterior Hox genes, which was rescued by the knockdown of let-7. These results suggest that the Lin28/let-7 pathway is involved in the modulation of the 'Hox code' via Polycomb regulation during axial patterning.

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DNA methylation increases nucleosome compaction and rigidity.

Project description:Cytosine methylation on CpG dinucleotides is an essential epigenetic modification in eukaryotes. How DNA methylation modulates nucleosome structure and dynamics has been a long-standing question. We implemented a single-molecule method to monitor the effects of DNA methylation on the structure and dynamics of mononucleosomes. Our studies show that DNA methylation induces a more compact and rigid nucleosome structure, providing a physical basis for how DNA methylation might contribute to regulating chromatin structure.

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