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Loss of CREBBP results in H3K27ac loss at enhancers in mouse lymphoma cells

ABSTRACT: KD of Crebbp at mouse cells results in reduced H3K27ac enrichment at a subset of promoters and enhancers.

ORGANISM(S): Mus musculus

PROVIDER: GSE79640 | GEO | 2016/10/13

SECONDARY ACCESSION(S): PRJNA316576

REPOSITORIES: GEO

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Loss of CREBBP results in H3K27ac loss at enhancers in lymphoma cells

Project description:KD of CREBBP at lymphoma cell line, MD901, results in reduced H3K27ac enrichment at a subset of promoters and enhancers.

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Loss of CREBBP results in gene expression represssion in mouse lymphoma cells

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Loss of CREBBP results in H3K27Ac loss at enhancers and gene expression repression in lymphoma cells

Project description:Loss of CREBBP results in H3K27Ac loss at enhancers and gene expression repression in lymphoma cells

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Loss of CREBBP results in H3K27Ac loss at enhancers and gene expression repression in lymphoma cells

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

2016-10-13 | GSE79686 | GEO

H3K27Ac mapping in isogenic CREBBP-WT, CREBBP-KO and EP300-KO SUDHL4 cell lines

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Regulation of Histone Acetylation by SUMOylation Through TFAP2C Binding to the Chromatin and Recruitment of HDAC Complex

Project description:Enhancers are fundamental to gene regulation. Post-translational modifications by the small ubiquitin-like modifiers (SUMO) modify chromatin regulation enzymes, including histone acetylases and deacetylases. However, it remains unclear whether SUMOylation regulates enhancer marks, acetylation at the 27th lysine residue of the histone H3 protein (H3K27Ac). We hypothesize that SUMOylation regulates H3K27Ac. To test this hypothesis, we performed genome-wide ChIP-seq analyses. We discovered that knockdown (KD) of the SUMO activating enzyme catalytic subunit UBA2 reduced H3K27Ac at most enhancers. Bioinformatic analysis revealed that TFAP2C-binding sites are enriched in enhancers whose H3K27Ac was reduced by UBA2 KD. ChIP-seq analysis in combination with molecular biological methods showed that TFAP2C binding to enhancers increased upon UBA2 KD or inhibition of SUMOylation by a small molecule SUMOylation inhibitor. However, this is not due to the SUMOylation of TFAP2C itself. Proteomics analysis of TFAP2C interactome on the chromatin identified histone deacetylation (HDAC) machinery. TFAP2C KD reduced HDAC binding to chromatin and increased H3K27Ac marks at enhancer regions, suggesting that TFAP2C is involved in recruiting HDAC. Taken together, our findings provide important insights into regulation of enhancer marks by SUMOylation.

2024-04-13 | PXD045644 | Pride

H3K27Ac mapping in isogenic CREBBP-WT, CREBBP-KO and EP300-KO SUDHL4 cell lines

Project description:Inactivating mutations of the CREBBP acetyltransferase and, at lower frequencies, its paralogue EP300 are among the most common genetic alterations in diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL), the two most frequent B cell malignancies. Here we uncover unexpected distinct functions for CREBBP and EP300 in the germinal center (GC), i.e. the target structure for most human B cell lymphomas. We show that these proteins modulate non-overlapping transcriptional programs that are preferentially enriched in biological functions associated with the separate anatomic compartments of the GC. Consistently, deletion of CREBBP or EP300 have opposing effects on GC formation in vivo. Nonetheless, these proteins partially compensate for each other to maintain a minimal threshold of acetyltransferase activity and guarantee homeostatic control of the GC, which is completely abrogated by their combined loss. This synthetic lethal interaction is retained in DLBCL cells, identifying an Achille’s heel in CREBBP-mutant lymphomas that could be pharmacologically targeted by using a novel, selective small molecule inhibitor of the CREBBP/EP300 bromodomain. These data shed light on the unique roles of CREBBP and EP300 in the physiology and pathology of GC B cells, and provide a proof-of-principle for the development and testing of EP300 inhibition as a therapeutic strategy in these diseases.

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