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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE36222 | GEO | 2012/11/30

SECONDARY ACCESSION(S): PRJNA153127

REPOSITORIES: GEO

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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

Microarray Samples for shACTL6A in HNSCC Cells to Investigate How ACTL6A and p63 Activate Hippo-YAP in SCC

Project description:Loss-of-function mutations in SWI/SNF chromatin remodeling subunit genes are observed in many cancers, but an oncogenic role for SWI/SNF is not well established. Here we reveal that ACTL6A, encoding a SWI/SNF subunit linked to stem and progenitor cell function, is frequently co-amplified and highly expressed together with the p53 family member p63 in head and neck squamous cell carcinoma (HNSCC). ACTL6A and p63 physically interact and cooperatively control a transcriptional program that promotes proliferation and suppresses differentiation, in part through activation of the Hippo-YAP pathway via regulators including WWC1. Consequently, loss of ACTL6A or p63 in tumor cells induces YAP phosphorylation and inactivation, associated with growth arrest and terminal differentiation, all phenocopied by WWC1 overexpression. In vivo, ectopic ACTLC6A/p63 expression promotes tumorigenesis, while ACTL6A expression and YAP activation are highly correlated in primary HNSCC and predict poor patient survival. Thus, ACTL6A and p63 collaborate as oncogenic drivers in HNSCC. Gene expression profiling of HNSCC cells with and without ablated endogenous ACTL6A via lentiviral shRNA.

2016-11-18 | GSE88831 | GEO

ChIP-Seq Samples for p63 in HNSCC Cells to Investigate How ACTL6A and p63 Activate Hippo-YAP in SCC

2016-11-18 | GSE88859 | GEO

Microarray Samples for shTP63 in HNSCC Cells to Investigate How ACTL6A and p63 Activate Hippo-YAP in SCC

2016-11-18 | GSE88833 | GEO

Microarray Samples for shTP63 in Immortalized HFK to Investigate How ACTL6A and p63 Activate Hippo-YAP in SCC

Project description:Loss-of-function mutations in SWI/SNF chromatin remodeling subunit genes are observed in many cancers, but an oncogenic role for SWI/SNF is not well established. Here we reveal that ACTL6A, encoding a SWI/SNF subunit linked to stem and progenitor cell function, is frequently co-amplified and highly expressed together with the p53 family member p63 in head and neck squamous cell carcinoma (HNSCC). ACTL6A and p63 physically interact and cooperatively control a transcriptional program that promotes proliferation and suppresses differentiation, in part through activation of the Hippo-YAP pathway via regulators including WWC1. Consequently, loss of ACTL6A or p63 in tumor cells induces YAP phosphorylation and inactivation, associated with growth arrest and terminal differentiation, all phenocopied by WWC1 overexpression. In vivo, ectopic ACTLC6A/p63 expression promotes tumorigenesis, while ACTL6A expression and YAP activation are highly correlated in primary HNSCC and predict poor patient survival. Thus, ACTL6A and p63 collaborate as oncogenic drivers in HNSCC. Gene expression profiling of untransformed keratinocytes (HaCaT) with and without ablated endogenous p63 via lentiviral shRNA.

2016-11-18 | GSE88832 | GEO

CUT&Tag result of ACTL6A, BRG1 and NRF2 related site in SNU638 gastric cancer cell line

Project description:ACTL6A has been identified as a transcriptional regulator and driving pathways that are of specific benefit to the malignant elements within the tumor. Here, we aimed to find genes that are regulated by ACTL6A by CUT&Tag. BRG1 is the catalytic subunit of the SWI/SNF chromatin-remodeling complex. Nuclear factor (erythroid-derived 2)-like 2 (NFE2L2, NRF2) is a transcription factor that governs the antioxidant pathway. IgG was used as a control.

2023-04-20 | GSE216350 | GEO

ACTL6a knockout peripheral nerve RNA seq at postnatal day 3

Project description:Cells need to integrate chemical and physical signals into transcriptional programs. In the peripheral nerves, axonal caliber selection by specialized Schwann cells, is critical for developmental myelination. However, only mechanisms through which Schwann cells sense chemical signals are well characterized. We identify ACtin-Like protein 6a (ACTL6a), a component of the SWI/SNF chromatin remodeling complex, as critical for axonal caliber recognition and developmental myelination. ACTL6a is expressed in the developing nerve and, when activated by contact with axons or nanofibers of specific caliber, it promotes the eviction of repressive histone marks thereby enhancing the transcriptional program of myelination. Mutant mice with Schwann cells lacking ACTL6a display aberrant recognition of axonal caliber, resulting in defective radial sorting and lower levels of transcripts regulating myelination of developing nerves. We suggest that developing peripheral nerves require an ACTL6a-dependent integration of physical and chemical signals in Schwann cells to release of repressive histone modifications and promote myelination.

2022-03-08 | GSE179340 | GEO

Homo sapiens

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

| PRJNA153127 | ENA

Baf53a is involved in survival of mouse ES cells, which can be compensated by Baf53b.

Project description:The human Baf (Brg1/Brm associated factor) complex, also known as the mammalian SWI/SNF chromatin-remodeling complex, is involved in a variety of cellular processes. The pluripotency and self-renewal abilities are major characteristics of embryonic stem (ES) cells and are regulated by the ES cell-specific BAF (esBAF) complex. Baf53a is one of the subunits of the esBAF complex. Here, we found that growth of Baf53a-deficient ES cells was repressed, and expression of p53, p21, and cleaved Caspase 3 was increased. Interestingly, Baf53b, a homologue of Baf53a, rescued cell death of Baf53a-deficient ES cells. Baf53a-deficient ES cells overexpressing exogenous Baf53a or Baf53b remained in the undifferentiated state and proliferated. In summary, our findings suggest that Baf53a is involved in the survival of ES cells, and that Baf53b is able to compensate for this functional aspect of Baf53a.

2017-11-16 | GSE103694 | GEO

Expression data from Knockdown of BAF53A in DLD1 cell line

Project description:BAF53A, an important subunit of the SWI/SNF epigenetic chromatin regulatory complex, has been implicated as the driver of diverse cancers. However, the role of BAF53A in colorectal cancer (CRC) remains poorly understood.

2022-12-21 | GSE218008 | GEO

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