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TFIIIC and MYCN link the three-dimensional chromatin structure of promoters to transcription termination of stalled RNA polymerase (RNA-Seq)

ABSTRACT: TFIIIC and MYCN link the three-dimensional chromatin structure of promoters to transcription termination of stalled RNA polymerase (RNA-Seq)

PROVIDER: PRJNA924772 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23099482_1.fastq.gz	Fastqsanger.gz
	SRR23099482_2.fastq.gz	Fastqsanger.gz
	SRR23099483_1.fastq.gz	Fastqsanger.gz
	SRR23099483_2.fastq.gz	Fastqsanger.gz
	SRR23099484_1.fastq.gz	Fastqsanger.gz

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TFIIIC and MYCN link the three-dimensional chromatin structure of promoters to transcription termination of stalled RNA polymerase (ChIPseq CnR)

Project description:MYC proteins bind to virtually all active promoters transcribed by RNA polymerase II (RNAPII), but whether they interact with the three-dimensional chromatin architecture is unknown. Here we used HiChIP sequencing of the MYCN oncoprotein and found that MYCN localizes to three-dimensional hubs formed by active promoters and enhancers. In these hubs, MYCN interacts with TFIIIC, an architectural protein complex. MYCN recruits TFIIIC to promoters when transcription elongation is inhibited, and the complex of both proteins induces premature transcription termination. Termination correlates closely with the TFIIIC-dependent removal of MYCN from promoter hubs and with corresponding alterations in the three-dimensional interactions of cohesin complexes. This limits DNA damage by removing RNAPII that stalls proximal to double-strand breaks. Binding of TFIIIC to MYCN is limited by competition with Aurora-A and this protects genes involved in mRNA processing from termination, arguing that MYCN contributes to the unusual proliferative capacity of neuroblastoma cells via removing stalled RNAPII from promoter hubs and via increasing the capacity for RNA processing.

2024-07-15 | GSE223052 | GEO

TFIIIC and MYCN link the three-dimensional chromatin structure of promoters to transcription termination of stalled RNA polymerase (HiC HiChIP)

2024-07-15 | GSE223054 | GEO

TFIIIC and MYCN link the three-dimensional chromatin structure of promoters to transcription termination of stalled RNA polymerase (RNA-Seq)

2024-07-15 | GSE223057 | GEO

TFIIIC and MYCN link the three-dimensional chromatin structure of promoters to transcription termination of stalled RNA polymerase

Project description:TFIIIC and MYCN link the three-dimensional chromatin structure of promoters to transcription termination of stalled RNA polymerase

| PRJNA924767 | ENA

TFIIIC and MYCN link the three-dimensional chromatin structure of promoters to transcription termination of stalled RNA polymerase (HiC HiChIP)

Project description:TFIIIC and MYCN link the three-dimensional chromatin structure of promoters to transcription termination of stalled RNA polymerase (HiC HiChIP)

| PRJNA924773 | ENA

TFIIIC and MYCN link the three-dimensional chromatin structure of promoters to transcription termination of stalled RNA polymerase (ChIPseq CnR)

Project description:TFIIIC and MYCN link the three-dimensional chromatin structure of promoters to transcription termination of stalled RNA polymerase (ChIPseq CnR)

| PRJNA924775 | ENA

TFIIIC and MYCN link the three-dimensional chromatin structure of promoters to transcription termination of stalled RNA polymerase

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

2024-07-15 | GSE223058 | GEO

Recruitment of BRCA1 limits MYCN-driven accumulation of stalled RNA Polymerase in neuroblastoma

Project description:Deregulation of the MYCN gene drives the development of neuronal and neuroendocrine tumors and is often associated with a particularly poor prognosis. Here we show that activation of MYCN in human neuroblastoma cells induces promoter escape of RNAPII. If pause release of RNAPII fails, MYCN recruits the BRCA1 protein to promoter-proximal regions. Recruitment of BRCA1 prevents MYCN-dependent accumulation of stalled RNAPII and enhances transcriptional activation by MYCN. Mechanistically, BRCA1 stabilizes mRNA de-capping complexes and enables MYCN to suppress R-loop formation in promoter-proximal regions. Recruitment of BRCA1 is mediated by the ubiquitin-specific protease, USP11, which binds specifically to MYCN that is de-phosphorylated at Thr58. Thr58 phosphorylation promotes proteasomal turnover of MYCN, hence BRCA1 stabilizes chromatin association of MYCN. Since BRCA1 is highly expressed in neuronal progenitor cells during early development and since MYC is less efficient than MYCN in recruiting BRCA1, our findings argue that a cell lineage-specific stress response enables MYCN-driven tumors to cope with deregulated RNAPII function.

2019-03-21 | GSE111905 | GEO

Recruitment of BRCA1 limits MYCN-driven accumulation of stalled RNA Polymerase in neuroblastoma

Project description:Recruitment of BRCA1 limits MYCN-driven accumulation of stalled RNA Polymerase in neuroblastoma

| PRJNA438512 | ENA

Stress-induced multimerization of MYC shields stalled replication forks from RNA Polymerase

Project description:Oncoproteins of the MYC family drive the development of numerous human tumors1-4. In unperturbed cells, MYC proteins bind to virtually all active promoters and control transcription by RNA Polymerase II (RNAPII)2,3,5,6. MYC proteins can also coordinate transcription with DNA replication7-9 and promote the repair of transcription-associated DNA damage10, but how they exert these mechanistically diverse functions is unknown. Here we show that MYC dissociates from most of its binding sites in promoters and forms stable multimeric shell-like structures in response to perturbation of transcription elongation, mRNA splicing, or DNA replication. MYC multimers recruit interacting proteins that can promote transcription termination into their shells. Intriguingly, MYC multimers accumulate on chromatin immediately adjacent to stalled replication forks and surround the FANCD2, ATR and BRCA1 proteins, which are located at stalled forks11,12. MYC multimers accumulate ubiquitylated proteins and their formation depends on the HUWE1 ubiquitin ligase10,13. In response to replication stress, HUWE1 and MYC limit phosphorylation of the single-strand binding protein, RPA. We propose that localised multimerisation of MYC creates a transcription termination zone around stalled replication forks that limits checkpoint signalling in response to transcriptional and replication stress, allowing tumor cells to actively proliferate under stressful conditions

2022-09-08 | GSE183094 | GEO

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