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CREB mediates transient and sustained genomic responses to cAMP via distinct mechanisms [ChIP-seq]

ABSTRACT: CREB mediates transient and sustained genomic responses to cAMP via distinct mechanisms [ChIP-seq]

PROVIDER: PRJNA522364 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8574020.fastq.gz	Fastqsanger.gz
	SRR8574030.fastq.gz	Fastqsanger.gz
	SRR8574040.fastq.gz	Fastqsanger.gz
	SRR8574050.fastq.gz	Fastqsanger.gz
	SRR8574060.fastq.gz	Fastqsanger.gz

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CREB mediates transient and sustained genomic responses to cAMP via distinct mechanisms [RNA-seq]

Project description:We investigated genome-wide occupancy of CREB, CREB coactivators, lineage determining transcription factors and histone acetylation to uncover mechanisms behind tissue-specific gene induction by cAMP in pancreatic islets. CREB mediates effects of cAMP on cellular gene expression. Most core CREB target genes are ubiquitously induced following recruitment of CREB and its coactivators to promoter proximal binding sites. We found that CREB stimulates the expression of pancreatic beta cell genes by binding to sites within distal enhancers. By contrast with its transient effects on core target genes, CREB stimulates pancreatic beta cell specific gene expression in a sustained manner, reflecting increases in the CBP-mediated acetylation of resident nucleosomes that recruit the chromatin reader BRD4. CREB cooperates with the lineage specific activator Neurod1 in establishing cAMP-responsive enhancers in beta cells. As deletion of a CREB-Neurod1 bound enhancer within the Lrrc10b-Syt7 super-enhancer locus disrupted the expression of both genes and decreased glucose-induced insulin secretion, our results demonstrate how cooperativity between signal dependent and lineage determining factors promotes the expression of cell type-specific gene programs in response to extracellular cues.

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CREB mediates transient and sustained genomic responses to cAMP via distinct mechanisms [ChIP-seq]

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CREB mediates transient and sustained genomic responses to cAMP via distinct mechanisms

Project description:CREB mediates transient and sustained genomic responses to cAMP via distinct mechanisms

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CREB mediates transient and sustained genomic responses to cAMP via distinct mechanisms [RNA-seq]

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Chromatin immunoprecipitation of human cell lines to identify cAMP-response element binding protein (CREB) binding sites.

Project description:Hormones and nutrients often induce genetic programs via signaling pathways that interface with gene-specific activators. Activation of the cAMP pathway, for example, stimulates cellular gene expression by means of the PKA-mediated phosphorylation of cAMP-response element binding protein (CREB) at Ser-133. Here, we use genome-wide approaches to characterize target genes that are regulated by CREB in different cellular contexts. CREB was found to occupy approximately 4,000 promoter sites in vivo, depending on the presence and methylation state of consensus cAMP response elements near the promoter. The profiles for CREB occupancy were very similar in different human tissues, and exposure to a cAMP agonist stimulated CREB phosphorylation over a majority of these sites. Only a small proportion of CREB target genes was induced by cAMP in any cell type, however, due in part to the preferential recruitment of the coactivator CREB-binding protein to those promoters. These results indicate that CREB phosphorylation alone is not a reliable predictor of target gene activation and that additional CREB regulatory partners are required for recruitment of the transcriptional apparatus to the promoter.

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CREB mediates transient and sustained genomic responses to cAMP via distinct mechanisms

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

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Defining a role for GPCR/cAMP/Creb signaling in HFSC activation

Project description:Our study demonstrates direct evidence that canonical cAMP/Creb signaling through adrenergic receptors can regulate HFSC activation and the hair cycle. This intracellular signaling circuit connects to downstrean glycolytic metabolism processes which have been previously shown to stimulate HSFC activation.

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Defining a role for GPCR/cAMP/Creb signaling in HFSC activation

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Characterize CREB target genes in different tissue types

Project description:The CREB family of transcription factors stimulates cellular gene expression following phosphorylation at a conserved serine (Ser133 in CREB1) in response to cAMP and other extracellular signals. In order to characterize CREB target genes in various tissues, we give a cAMP agonist, forskolin (FSK), to cell lines or primary cultures and monitor the gene expression. To eliminate CREB-independent effects of FSK on cellular gene expression, we employed a dominant negative form of CREB called A-CREB, which dimerizes selectively with and blocks the DNA binding activity of CREB but not other bZIP family members. Therefore, genes that are induced by cAMP and the induction was blocked by A-CREB treatment likely represents CREB target genes. Notes: 1) In HEK293T cells, besides the Control+FSK+(FSK-ACREB) experiments, a different set of experiments showing FSK effect on 1hr and 4hr is included. The two sets of data in HEK293T were generated at different times with different batch of cells, and comparison should be limited within each set. The cAMP induced genes at 1hr, however, was similar between the two sets. 2) These is no ACREB data for pancreatic islets or hepatocytes. For hepatocytes, however, we have included fasting liver and refed liver in additional to FSK treated primary hepatocytes. During fasting, glucagon induces cAMP increase in the liver and CREB is activated. Therefore, a more reliable list of CREB target genes in hepatocytes can be obtained by selecting those genes are that induced both during fasting and in FSK treated primary culture. Keywords: parallel sample

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