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PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression [ChIP-seq]

ABSTRACT: PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression [ChIP-seq]

PROVIDER: PRJNA748396 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15201724.fastq.gz	Fastqsanger.gz
	SRR15201725.fastq.gz	Fastqsanger.gz
	SRR15201726.fastq.gz	Fastqsanger.gz
	SRR15201727.fastq.gz	Fastqsanger.gz
	SRR15201728.fastq.gz	Fastqsanger.gz

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PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression

Project description:PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression

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PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression[CUT&RUN]

Project description:Genes encoding subunits of SWI/SNF chromatin remodeling complexes are mutated in nearly 25% of cancers. The SWI/SNF subunit SMARCB1 is the driving mutation in nearly all cases of rhabdoid tumor (RT), highly malignant cancers of childhood. While loss of SMARCB1 drives cancer, its absence also creates unique dependencies, which can illuminate mechanism and reveal potential therapeutic vulnerabilities. To identify such dependencies we undertook a genome-scale CRISPR screen comparing RT cell lines to 800 other cancer lines. We identified PHF6 as specifically essential for RT cell survival. Germline mutations in both SMARCB1 and PHF6 cause Coffin-Siris syndrome, and somatic mutations in PHF6 or SWI/SNF occur in T-ALL, suggesting a mechanistic link. We establish that PHF6 co-localizes with residual SWI/SNF complexes at active promoters and enhancers. We find that PHF6 is specifically required for H3K14ac accumulation immediately downstream of active promoters and for release of paused Pol II. Collectively, our work identifies novel integrated roles for PHF6 in chromatin and Pol II regulation, establishes a mechanistic basis for dependence upon PHF6 in RT, and reveals a novel potential therapeutic vulnerability in RT.

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PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression [ChIP-seq]

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PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression [ATAC-seq]

Project description:Genes encoding subunits of SWI/SNF(BAF) chromatin remodeling complexes are collectively mutated in nearly 25% of all cancers. Utilizing a genome-wide CRISPR-Cas9 screen, we identify PHF6 as a specific vulnerability in pediatric malignant rhabdoid tumors (RTs), which are driven by inactivation of the SMARCB1 subunit of SWI/SNF. We establish that PHF6 co-localizes with residual SWI/SNF subcomplexes at promoters and enhancers. Here, PHF6 facilitates transcriptional activation by regulating deposition of H3K14ac downstream of active promoters and contributes to the establishment of H3K27ac at active promoters and enhancers. We show that PHF6 is essential for the maintenance of these marks in part via the regulation of their writers, HB01 and CBP/p300, respectively. As it directly regulates the H3K14ac mark, PHF6 may regulate pausing and serve as a mediator between chromatin regulatory function and RNA POL II pause release. Together, our results establish a mechanistic basis for dependence upon PHF6 in SMARCB1-mutant RTs.

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PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression [RNA-seq]

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PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression [RNA-seq]

Project description:PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression [RNA-seq]

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PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression[CUT&RUN]

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PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression [ATAC-seq]

Project description:PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression [ATAC-seq]

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PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression.

Project description:Genes encoding subunits of SWI/SNF (BAF) chromatin remodeling complexes are mutated in nearly 25% of cancers. To gain insight into the mechanisms by which SWI/SNF mutations drive cancer, we contributed ten rhabdoid tumor (RT) cell lines mutant for SWI/SNF subunit SMARCB1 to a genome-scale CRISPR-Cas9 depletion screen performed across 896 cell lines. We identify PHF6 as specifically essential for RT cell survival and demonstrate that dependency on Phf6 extends to Smarcb1-deficient cancers in vivo. As mutations in either SWI/SNF or PHF6 can cause the neurodevelopmental disorder Coffin-Siris syndrome, our findings of a dependency suggest a previously unrecognized functional link. We demonstrate that PHF6 co-localizes with SWI/SNF complexes at promoters, where it is essential for maintenance of an active chromatin state. We show that in the absence of SMARCB1, PHF6 loss disrupts the recruitment and stability of residual SWI/SNF complex members, collectively resulting in the loss of active chromatin at promoters and stalling of RNA Polymerase II progression. Our work establishes a mechanistic basis for the shared syndromic features of SWI/SNF and PHF6 mutations in CSS and the basis for selective dependency on PHF6 in SMARCB1-mutant cancers.

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PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression

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

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