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KAP1 regulates elongation kinetics to activate signal-induced transcription

ABSTRACT: KAP1 regulates elongation kinetics to activate signal-induced transcription

PROVIDER: PRJNA1032052 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28919400_1.fastq.gz	Fastqsanger.gz
	SRR28919400_2.fastq.gz	Fastqsanger.gz
	SRR28919401_1.fastq.gz	Fastqsanger.gz
	SRR28919401_2.fastq.gz	Fastqsanger.gz
	SRR28919402_1.fastq.gz	Fastqsanger.gz

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KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [ChIP-Seq]

Project description:KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [ChIP-Seq]

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KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [RNA-Seq]

Project description:KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [RNA-Seq]

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KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [PRO-Seq]

Project description:KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [PRO-Seq]

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KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [TT-Seq]

Project description:KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [TT-Seq]

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KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [PRO-Seq]

Project description:Signal-induced transcriptional programs regulate critical biological processes through the precise spatiotemporal activation of Immediate Early Genes (IEGs); however, the mechanisms of transcription induction are still unfolding. By combining an acute depletion system with high resolution genomics approaches to interrogate synchronized, temporal transcription, we reveal that KAP1/TRIM28 is a first responder that fulfills the temporal and heightened transcriptional demand of IEGs. Unexpectedly, acute KAP1 loss triggers an increase in RNA Polymerase II elongation kinetics during early stimulation time points. This elongation defect derails the normal progression through the transcriptional cycle during late stimulation time points, ultimately leading to decreased recruitment of the transcription apparatus for re-initiation and dampening IEG transcription. Collectively, KAP1 plays a counterintuitive role by negatively regulating transcription elongation to support full activation across multiple transcription cycles of genes critical for cell physiology and organismal functions.

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KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [TT-Seq]

2024-05-07 | GSE266694 | GEO

KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [RNA-Seq]

2024-05-07 | GSE266693 | GEO

KAP1 negatively regulates elongation kinetics to activate signal-induced transcription [ChIP-Seq]

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KAP1 regulates elongation kinetics to activate signal-induced transcription

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

2024-05-07 | GSE246218 | GEO

An eRNA Transcription Checkpoint For Diverse Signal-dependent Enhancer Activation Programs

Project description:While many or most signal and ligand-dependent pathways function by directing binding of specific transcription factors to large cohorts of regulatory enhancers, the possible “universal” strategies underling activation of these lorge enhancer programs by diverse signals remains poorly understood. Here, we report that ligands, exemplified by estrogen-17-b (E2), cause the recruitment of DNA-PKcs-phosphorylated KAP1 to estrogen receptor a (ERa)-bound enhancers, inhibiting its E3 SUMO ligase activity for the CDK9 subunit of P-TEFb, which permits formation of active P-TEFb required for eRNA elongation overcoming this checkpoint and permitting enhancer activation. We find that most, or all, signal and ligand enhancer activation programs similarly require the loss of SUMOligase function by phoshorylation of KAP1 to prevent Pol II pausing at regulated enhancers. This is based on activation of P-TEFb consequent to deSUMOylation of CDK9, permitting eRNA synthesis. Overcoming this checkpoint appears to be a widely, if not universally, used strategy for signal-dependent enhancer activation because similar events occur on AR and NF-kB-regulated enhancers and even following depolarization acutely-activated neuronal enhancers. This study reveals an unexpected strategy required to overcome a checkpoint common to most or all signal/ligand-regulated enhancers critical to activate broad programs of biologically-important regulatory enhancers that implement the instructions of the endocrine system.

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