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Dissecting the regulatory strategies of NFkB RelA target genes in the inflammatory response reveals differential transactivation logics

ABSTRACT: Dissecting the regulatory strategies of NFkB RelA target genes in the inflammatory response reveals differential transactivation logics

PROVIDER: PRJNA548321 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10529434.fastq.gz	Fastqsanger.gz
	SRR10529435.fastq.gz	Fastqsanger.gz
	SRR10529436.fastq.gz	Fastqsanger.gz
	SRR10529437.fastq.gz	Fastqsanger.gz
	SRR9285990.fastq.gz	Fastqsanger.gz

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Dissecting the regulatory strategies of NFkB RelA target genes in the inflammatory response reveals differential transactivation logics

Project description:NFkB RelA is the potent transcriptional activator of inflammatory response genes. We stringently defined a list of direct RelA target genes by integrating physical (ChIPseq) and functional (RNAseq in knockouts) datasets. We then dissected each gene's regulatory strategy by testing RelA variants in a novel primary-cell genetic complementation assay. All endogenous target genes required that RelA makes DNA-base-specific contacts, and none could be activated by the DNA binding domain alone. However, endogenous target genes differed widely in how they employ the two transactivation domains. Through model-aided analysis of the dynamic timecourse data we reveal gene-specific synergy and redundancy of TA1 and TA2. Given that post-translational modifications control TA1 activity and intrinsic affinity for coactivators determines TA2 activity, the differential TA logics suggests context-dependent vs. context-independent control of endogenous RelA-target genes. While some inflammatory initiators appear to require co-stimulatory TA1 activation, inflammatory resolvers are a part of the NFkB RelA core response.

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Project description:NFkB RelA is the potent transcriptional activator of inflammatory response genes. We stringently defined a list of direct RelA target genes by integrating physical (ChIPseq) and functional (RNAseq in knockouts) datasets. We then dissected each gene’s regulatory strategy by testing RelA variants in a novel primary-cell genetic complementation assay. All endogenous target genes required that RelA makes DNA-base-specific contacts, and none could be activated by the DNA binding domain alone. However, endogenous target genes differed widely in how they employ the two transactivation domains. Through model-aided analysis of the dynamic timecourse data we reveal gene-specific synergy and redundancy of TA1 and TA2. Given that post-translational modifications control TA1 activity and intrinsic affinity for coactivators determines TA2 activity, the differential TA logics suggests context-dependent vs. context-independent control of endogenous RelA-target genes. While some inflammatory initiators appear to require co-stimulatory TA1 activation, inflammatory resolvers are a part of the NFkB RelA core response.

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Project description:Dissecting the regulatory strategies of NFkB RelA target genes in the inflammatory response reveals differential transactivation logics

| PRJNA549287 | ENA

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