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CBP is required for establishing adaptive gene programs in the adult brain [ChIP-seq]

ABSTRACT: We investigated the impact in transcription, chromatin acetylation and behavior of eliminating either CBP or p300 in excitatory neurons of the adult forebrain. The elimination of CBP reduced the expression of plasticity genes. The importance of CBP became more prominent in paradigms that involved a chronic or recurrent change in transcription, including kindling and neuroadaptation to environmental enrichment, in which CBP loss interfered with the establishment of activity-induced transcriptional and epigenetic adaptive changes in response to stimulus or experience. Comparative analyses in mice lacking CBP’s paralog p300 underscored the specificity of CBP function.

ORGANISM(S): Mus musculus

PROVIDER: GSE200591 | GEO | 2022/11/17

REPOSITORIES: GEO

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CBP is required for establishing adaptive gene programs in the adult brain [p300]

Project description:We investigated the impact in transcription, chromatin acetylation and behavior of eliminating either CBP or p300 in excitatory neurons of the adult forebrain. The elimination of CBP reduced the expression of plasticity genes. The importance of CBP became more prominent in paradigms that involved a chronic or recurrent change in transcription, including kindling and neuroadaptation to environmental enrichment, in which CBP loss interfered with the establishment of activity-induced transcriptional and epigenetic adaptive changes in response to stimulus or experience. Comparative analyses in mice lacking CBP’s paralog p300 underscored the specificity of CBP function.

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CBP is required for establishing adaptive gene programs in the adult brain [kindling]

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RNA binds to a CBP regulatory motif to stimulate histone acetylation and transcription

Project description:CBP/p300 are transcription co-activators whose binding is a signature of enhancers, cis-regulatory elements that control patterns of gene expression in multicellular organisms. Active enhancers produce bi-directional enhancer RNAs (eRNAs) and display CBP/p300 dependent histone acetylation. Here, we demonstrate that CBP binds directly to RNAs in vivo and in vitro. RNAs bound to CBP in vivo include a large number of eRNAs. Using steady-state histone acetyltransferase (HAT) assays we show that an RNA binding region in the HAT domain of CBP—a regulatory motif unique to CBP/p300—allows RNA to stimulate CBP’s HAT activity. At enhancers where CBP interacts with eRNAs, stimulation manifests in RNA-dependent changes in the histone acetylation mediated by CBP, such as H3K27ac, and by corresponding changes in gene expression. By interacting directly with CBP, eRNAs contribute to the unique chromatin structure at active enhancers, which in turn is required for regulation of target genes.

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Time-resolved analysis reveals rapid dynamics and broad scope of the CBP/p300 acetylome

Project description:The acetyltransferases CBP and p300 are multifunctional transcriptional co-activators; however, their acetylation targets, site-specific acetylation kinetics, and function in proteome regulation are incompletely understood. We combined quantitative proteomics with novel CBP/p300-specific catalytic inhibitors, bromodomain inhibitor, and gene knockout to show that CBP/p300 acetylates thousands of sites, including signature histone sites, as well as a multitude of sites on signaling effectors and enhancer-associated transcriptional regulators. Kinetic analysis identified a subset of CBP/p300-regulated sites with very rapid (<30min) acetylation turnover, revealing a dynamic balance between acetylation and deacetylation. Quantification of acetylation, mRNA, and protein abundance after CBP/p300 inhibition reveals a kinetically competent network of gene expression that strictly depends on CBP/p300-catalyzed rapid acetylation. Collectively, our in-depth acetylome analyses reveal systems attributes of CBP/p300 targets, and the resource dataset provides a framework for investigating CBP/p300 functions, as well as for understanding the impact of small molecule inhibitors targeting its catalytic and bromodomain activities.

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CREBBP (CBP) ChIP-seq in wild type and CBP null MEFs +/- dipyridyl

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