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Increased ACTL6A Occupancy Within mSWI/SNF Chromatin Remodelers Drives Human Squamous Cell Carcinoma

ABSTRACT: Increased ACTL6A Occupancy Within mSWI/SNF Chromatin Remodelers Drives Human Squamous Cell Carcinoma

PROVIDER: PRJNA659015 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12508500_1.fastq.gz	Fastqsanger.gz
	SRR12508500_2.fastq.gz	Fastqsanger.gz
	SRR12508501_1.fastq.gz	Fastqsanger.gz
	SRR12508501_2.fastq.gz	Fastqsanger.gz
	SRR12508502_1.fastq.gz	Fastqsanger.gz

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Increased ACTL6A occupancy within mSWI/SNF chromatin remodelers drives human squamous cell carcinoma.

Project description:Mammalian SWI/SNF (BAF) chromatin remodelers play dosage-sensitive roles in many human malignancies and neurologic disorders. The gene encoding the BAF subunit actin-like 6a (ACTL6A) is amplified early in the development of many squamous cell carcinomas (SCCs), but its oncogenic role remains unclear. Here we demonstrate that ACTL6A overexpression leads to its stoichiometric assembly into BAF complexes and drives their interaction and engagement with specific regulatory regions in the genome. In normal epithelial cells, ACTL6A was substoichiometric to other BAF subunits. However, increased ACTL6A levels by ectopic expression or in SCC cells led to near saturation of ACTL6A within BAF complexes. Increased ACTL6A occupancy enhanced polycomb opposition genome-wide to activate SCC genes and facilitated the co-dependent loading of BAF and TEAD-YAP complexes on chromatin. Both mechanisms appeared to be critical and function as a molecular AND gate for SCC initiation and maintenance, thereby explaining the specificity of the role of ACTL6A amplification in SCCs.

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ACTL6a Enforces the Epidermal Progenitor State by Suppressing SWI/SNF-Dependent Induction of KLF4

Project description:Somatic progenitors suppress differentiation to maintain tissue self-renewal. While epigenetic regulators of DNA and histone modifications can support such repression, a role for nuclear actin-like proteins is unclear. In epidermis, ACTL6a/BAF53A was found enriched in progenitors and down-regulated during differentiation. Conditional ACTL6a deletion abolished epidermal self-renewal and induced terminal differentiation, whereas ectopically expressed ACTL6a suppressed differentiation. Among known activators of epidermal differentiation, KLF4 was found to control 227 genes also regulated by ACTL6a. ACTL6a loss upregulated KLF4 and its target genes, effects that were blocked by KLF4 depletion. Among multiple ACTL6a-interacting epigenetic regulators, the SWI/SNF complex was required for KLF4 activation and differentiation. In progenitors, ACTL6a loss led to enhanced SWI/SNF binding to the promoters of KLF4 and other differentiation genes. ACTL6a thus maintains the undifferentiated progenitor state, in part by suppressing SWI/SNF complex-enabled induction of KLF4. Gene expression analysis: To identify the gene set controlled by ACTL6a in human keratinocyte. Total RNA was isolated in biologic duplicate from cells with ACTL6a loss as compared to controls, and hybridized to Affymetrix HG-U133 2.0 Plus arrays.

2012-11-30 | E-GEOD-36222 | biostudies-arrayexpress

Increased ACTL6A Occupancy Within mSWI/SNF Chromatin Remodelers Drives Human Squamous Cell Carcinoma

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

2021-10-29 | GSE156788 | GEO

Identifying the genomic regions co-bound by ASCL1 and mSWI/SNF remodelers during neural differentiation [ChIP-seq]

Project description:We interfeered with the ASCL1-mSWI/SNF interaction: to abolish ASCL1 function, we knocked out ASCL1 in human iPSCs, while we used the BRM014 inhibitor to block the mSWI/SNF ATPase activity. We then performed ASCL1 ChIPseq in DIV24 WT and BRM014-treated neural cultures, and SMARCB1 ChIPseq in DIV24 WT and ASCL1 KO neural cultures, when ASCL1 expression is highest.

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ACTL6a Enforces the Epidermal Progenitor State by Suppressing SWI/SNF-Dependent Induction of KLF4

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Identifying the genomic regions where ASCL1 and mSWI/SNF remodelers are both required to regulate chromatin accessibility during neural differentiation [ATAC-seq]

Project description:We interfeered with the ASCL1-mSWI/SNF interaction: to abolish ASCL1 function, we knocked out ASCL1 in human iPSCs, while we used the BRM014 inhibitor to block the mSWI/SNF ATPase activity. We performed ATACseq in WT, ASCL1 KO, and BRM014-treated cells at DIV24, when ASCL1 expression is highest during neural differentiation.

2023-03-14 | GSE214380 | GEO

Identifying the transcriptional output associated with distal regulatory elements where ASCL1 interacts with mSWI/SNF remodelers to regulate neural differentiation [RNA-seq]

Project description:We interfeered with the ASCL1-mSWI/SNF interaction: to abolish ASCL1 function, we knocked out ASCL1 in human iPSCs, while we used the BRM014 inhibitor to block the mSWI/SNF ATPase activity. We then collected RNA from WT, ASCL1 KO and BRM014-treated cells at DIV24, when ASCL1 expression is highest during neural differentiation.

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Project description:Identifying the genomic regions co-bound by ASCL1 and mSWI/SNF remodelers during neural differentiation [ChIP-seq]

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mSWI/SNF functional genomic characterization of SMARCB1 mutants in SMARCB1-null and heterozygous settings

Project description:Chromatin remodeling complexes regulate gene expression by shifting, evicting, and exchanging nucleosomes along the chromosomes of eukaryotic organisms. The mammalian SWI/SNF chromatin remodeling complex (mSWI/SNF or BAF) is mutated in over 20% of human cancers and loss of the SMARCB1 gene, encoding the BAF47 protein subunit, results in one of the most aggressive and lethal pediatric cancers. An accumulation of point mutations occurs at the C-terminal end of the protein, for which the functional ramifications are unknown. We previously demonstrated that reintroduction of SMARCB1 in SMARCB1-null malignant rhabdoid tumor cells results in a genome-wide increase of mSWI/SNF complex occupancy coupled with activation of PRC2-repressed genes. Here, we study the functional consequences that these point mutations exert on mSWI/SNF complex activity in SMARCB1-deficient tumor cells and extend this investigation to a CRISPR/Cas9-mediated SMARCB1-heterozygous mutant induced pluripotent stem cell. Intriguingly, we observe that the mutant complexes bind similarly to wild-type SMARCB1 complexes at enhancers throughout the genome but often fail to transcriptionally activate nearby genes in a cis-regulatory manner.

2019-11-21 | GSE124903 | GEO

Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [RNA-seq]

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2023-03-21 | GSE212353 | GEO

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