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SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia [RNA-seq]

ABSTRACT: SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia [RNA-seq]

PROVIDER: PRJNA784963 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17074500.fastq.gz	Fastqsanger.gz
	SRR17074501.fastq.gz	Fastqsanger.gz
	SRR17074502.fastq.gz	Fastqsanger.gz
	SRR17074485.fastq.gz	Fastqsanger.gz
	SRR17074486.fastq.gz	Fastqsanger.gz

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SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia [RNA-seq]

Project description:Histone methyltransferase SETD1A is critical for acute myeloid leukemia (AML) cell survival, but the molecular mechanism driving SETD1A gene regulation remains elusive. To delineate the role of SETD1A, we utilize a protein degrader technology to induce rapid SETD1A degradation in AML cell lines. SETD1A degradation results in immediate downregulation of transcripts associated with DNA repair and heme biosynthesis pathways. CRISPR-based functional analyses and metabolomics revealed an essential role of SETD1A to maintain mitochondrial respiration in AML cells. These SETD1A targets are enriched in head-to-head (H2H) genes. SETD1A degradation disturbs a non-enzymatic SETD1A domain-dependent cyclin K function, increases the mono-Ser5P RNA polymerase II (RNAP2) at TSS, and induces the promoter-proximal pausing of RNAP2 in a strand-specific manner. This study reveals a non-enzymatic role for SETD1A in transcriptional pause release and provides insight into the mechanism of RNAP2 pausing and its function in cancer.

2022-12-09 | GSE189893 | GEO

SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia [ChIP-Seq]

2022-12-09 | GSE190994 | GEO

SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia

Project description:SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia

| PRJNA784959 | ENA

SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia [ChIP-Seq]

Project description:SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia [ChIP-Seq]

| PRJNA789267 | ENA

SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia

Project description:Histone methyltransferase SETD1A is critical for acute myeloid leukemia (AML) cell survival, but the molecular mechanism driving SETD1A gene regulation remains elusive. To delineate the role of SETD1A, we utilize a protein degrader technology to induce rapid SETD1A degradation in AML cell lines. SETD1A degradation results in immediate downregulation of transcripts associated with DNA repair and heme biosynthesis pathways. CRISPR-based functional analyses and metabolomics reveal an essential role of SETD1A to maintain mitochondrial respiration in AML cells. These SETD1A targets are enriched in head-to-head (H2H) genes. SETD1A degradation disrupts a non-enzymatic SETD1A domain-dependent cyclin K function, increases the Ser5P RNA polymerase II (RNAP2) at TSS, and induces the promoter-proximal pausing of RNAP2 in a strand-specific manner. This study reveals a non-enzymatic role for SETD1A in transcriptional pause release and provides insight into the mechanism of RNAP2 pausing and its function in cancer.

2022-10-12 | ST002323 | MetabolomicsWorkbench

SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia.

Project description:Histone methyltransferase SETD1A is critical for acute myeloid leukemia (AML) cell survival, but the molecular mechanism driving SETD1A gene regulation remains elusive. To delineate the role of SETD1A, we utilize a protein degrader technology to induce rapid SETD1A degradation in AML cell lines. SETD1A degradation results in immediate downregulation of transcripts associated with DNA repair and heme biosynthesis pathways. CRISPR-based functional analyses and metabolomics reveal an essential role of SETD1A to maintain mitochondrial respiration in AML cells. These SETD1A targets are enriched in head-to-head (H2H) genes. SETD1A degradation disrupts a non-enzymatic SETD1A domain-dependent cyclin K function, increases the Ser5P RNA polymerase II (RNAPII) at the transcriptional start site (TSS), and induces the promoter-proximal pausing of RNAPII in a strand-specific manner. This study reveals a non-enzymatic role for SETD1A in transcriptional pause release and provides insight into the mechanism of RNAPII pausing and its function in cancer.

| S-EPMC9771694 | biostudies-literature

SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia

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

2022-12-09 | GSE189894 | GEO

Brd4 and JMJD6-associated Anti-pause Enhancers in Regulation of Transcriptional Pause Release

Project description:Distal enhancers characterized by H3K4me1 mark play critical roles in developmental and transcriptional programs. However, potential roles of specific distal regulatory elements in regulating RNA Polymerase II (Pol II) promoter-proximal pause release remain poorly investigated. Here we report that a unique cohort of jumonji C domain-containing protein 6 (JMJD6) and bromodomain-containing protein 4 (Brd4) co-bound distal enhancers, termed anti-pause enhancers (A-PEs), regulate promoter-proximal pause release of a large subset of transcription units via long-range interactions. Brd4-dependent JMJD6 recruitment on A-PEs mediates erasure of H4R3me2(s), which is directly read by 7SK snRNA, and decapping/demethylation of 7SK snRNA, ensuring the dismissal of the 7SKsnRNA/HEXIM inhibitory complex. The interactions of both JMJD6 and Brd4 with the P-TEFb complex permit its activation and pause release of regulated coding genes. The functions of JMJD6/ Brd4-associated dual histone and RNA demethylase activity on anti-pause enhancers have intriguing implications for these proteins in development, homeostasis and disease. All Gro-seq(s) were designed to reveal the transcriptional targets of JMJD6 and Brd4, and assess the role of JMJD6 and Brd4 in Pol II promoter-proximal pause release. All ChIP-seq(s) were designed to understand the unique features, associated molecular mechanisms and functions of the anti-pause enhancers (A-PEs) discovered in the current study.

2014-01-14 | E-GEOD-51633 | biostudies-arrayexpress

Myo6 regulate transcriptional pause release

Project description:Myo6 regulate transcriptional pause release

| PRJEB5777 | ENA

The PNUTS phosphatase complex controls transcription pause release

Project description:Gene expression is regulated by controlling distinct steps of the transcriptional cycle, including initiation, pausing, elongation, and termination. Kinases phosphorylate RNA Polymerase II and associated factors to control transitions between these steps and act as central gene regulatory nodes. Similarly, phosphatases that dephosphorylate these components are emerging as important regulators of transcription, though their roles remain less well understood. Here we discover that the PNUTS-PP1 phosphatase complex plays an essential role in controlling transcription pause release in addition to its previously described function in transcription termination. Transcription pause release by the PNUTS complex is essential for almost all RNA Pol II-dependent gene transcription, relies on its PP1 phosphatase subunit, and controls the phosphorylation of factors required for pause release and elongation. Together, this reveals an essential new role for a phosphatase complex in transcription pause release and shows that the PNUTS complex is essential for RNA Poll II-dependent transcription.

2024-06-28 | MSV000095177 | MassIVE

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