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MIB1-mediated H2AK119 mono-ubiquitination chromatin landscapes independent of canonical PRC1

ABSTRACT: Polycomb repressive complex 1 (PRC1) is a central regulator of transcriptional repression through RING1B-mediated mono-ubiquitination of histone H2A at lysine 119 (H2AK119ub). Recent studies have suggested that the E3 ubiquitin ligase MIB1, previously characterized in Notch signaling, may also contribute to H2AK119ub deposition through a PRC1-independent mechanism. To investigate the chromatin-associated roles of MIB1, we generated ChIP-seq datasets for MIB1, RING1B, and H2AK119ub in the human colorectal cancer cell line HCT116. These datasets enable comparative analysis of genome-wide binding patterns, identification of shared and distinct target regions, and assessment of PRC1-dependent and PRC1-independent modes of H2AK119ub regulation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE317825 | GEO | 2026/02/09

REPOSITORIES: GEO

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Project description:Two distinct Polycomb complexes, PRC1 and PRC2, collaborate to maintain epigenetic repression of key developmental loci in embryonic stem cells (ESCs). PRC1 and PRC2 have histone modifying activities, catalyzing mono-ubiquitination of histone H2A (H2AK119u1) and trimethylation of H3 lysine 27 (H3K27me3) respectively. Compared to H3K27me3, localization and role of H2AK119ub1 is not fully understood in ESCs. Here we present genome-wide H2AK119u1 maps in ESCs and identify a group of genes at which H2AK119u1 is deposited in a Ring1-dependent manner. These genes are a distinctive subset of genes with H3K27me3 enrichment and are the central targets of Polycomb silencing that are required to maintain ESC identity. We further show that the H2A ubiquitination activity of PRC1 is dispensable for its target binding and its activity to compact chromatin at Hox loci, but is indispensable for efficient repression of target genes and thereby ESC maintenance. These data demonstrate that multiple effector mechanisms including H2A ubiquitination and chromatin compaction combine to mediate PRC1-dependent repression of genes that are crucial for the maintenance of ESC identity. Utilization of these diverse effector mechanisms might provide a means to maintain a repressive state that is robust yet highly responsive to developmental cues during ES cell self-renewal and differentiation. This SuperSeries is composed of the following subset Series: GSE38224: Expression data from Ring1A(-/-);Ring1B(fl/fl);R26::CreERT2 ES cells expressing either of mock, WT or mutant Ring1B construct before or after OHT treatment GSE38504: ChIP-on-chip analysis of Ring1B, Ring1A, H2AK119u1 and H3K27me3 in mouse ES cells Total RNAs were extracted from the respective ES cells, and were subjected to microarray analysis using Affymetrix GeneChip Mouse Genome 430A 2.0 arrays. ChIP on chip analysis was carried out using the Mouse Promoter ChIP-on-chip Microarray Set (G4490A, Agilent, Palo Alto, Calif., USA). MEFs were subjected to ChIP assay using various antibodies. Purified immunoprecipitated and input DNA was subjected to T7 RNA polymerase-based amplification. Labeling, hybridization and washing were carried out according to the Agilent mammalian ChIP-on-chip protocol (ver.9.0). Scanned images were quantified with Agilent Feature Extraction software under standard conditions.

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MIB1-mediated H2AK119 mono-ubiquitination chromatin landscapes independent of canonical PRC1

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