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CTCF acetylation at lysine 20 is required for early cardiac mesoderm differentiation from embryonic stem cells [ChIP-Seq]

ABSTRACT: In this study, we show that CTCF could be acetylated at lysine 20 (CTCF-K20) by CREB binding protein (CBP) and deacetylated by HDAC6, respectively. CTCF-K20 is required for CTCF interacting with CBP. CTCF point mutation at K20 has no effect on self-renewal but blocks mesoderm differentiation of mouse embryonic stem cells (mESCs).

ORGANISM(S): Mus musculus

PROVIDER: GSE181703 | GEO | 2022/10/24

REPOSITORIES: GEO

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CTCF acetylation at lysine 20 is required for early cardiac mesoderm differentiation from embryonic stem cells [ATAC-Seq]

Project description:In this study, we show that CTCF could be acetylated at lysine 20 (CTCF-K20) by CREB binding protein (CBP) and deacetylated by HDAC6, respectively. CTCF-K20 is required for CTCF interacting with CBP. CTCF point mutation at K20 has no effect on self-renewal but blocks mesoderm differentiation of mouse embryonic stem cells (mESCs).

2022-10-24 | GSE181702 | GEO

CTCF acetylation at lysine 20 is required for early cardiac mesoderm differentiation from embryonic stem cells [RNA-Seq]

2022-10-24 | GSE181704 | GEO

CTCF acetylation at lysine 20 is required for early cardiac mesoderm differentiation from embryonic stem cells [BL-Hi-C]

2022-10-24 | GSE181700 | GEO

Targeting HDAC6-Mediated Deacetylation of STAT4 Is Critical for T helper Type 1 Cell Differentiation and Capability

Project description:We report that inhibition and knockout of HDAC6 enhanced Th1 cell differentiation, and decreased Listeria monocytogenes infection in mice. Mechanistically, HDAC6 directly deacetylated CBP-catalyzed acetylation on STAT4 lysine 667 via its enzymatic activity, which is required for IL-12-induced phosphorylation on STAT4. Stat4K667R mutant mice lost the ability to normally differentiate Th1 cell and developed sever L. monocytogenes infection. Our study identifies the STAT4 acetylation on K667 modified dynamically by CBP and HDAC6, as an essential signaling event for Th1 cell differentiation and defense of intracellular pathogen infections, highlighting the therapeutic potential of HDAC6 inhibition for controlling intracellular pathogen infections.

2022-12-15 | GSE146253 | GEO

ARID1A-mutated ovarian cancers depend on HDAC6 activity

Project description:ARID1A, encoding a subunit of the SWI/SNF chromatin remodeling complex, is the most mutated epigenetic regulator in human cancers. ARID1A and TP53 mutations are typically mutually exclusive. Therapeutic approaches that correlate with ARID1A mutational status remain a challenge. Here, we show that HDAC6 activity is essential in ARID1A-mutated ovarian cancers. Inhibition of HDAC6 activity using a clinically applicable small molecule inhibitor significantly improved the survival of mice bearing ARID1A-mutated ovarian tumors. This correlated with the suppression of growth and dissemination of ARID1A-mutated, but not wild-type, tumors. The dependence on HDAC6 activity in ARID1A-mutated cells correlated with a direct transcriptional repression of HDAC6 by ARID1A. HDAC6 inhibition selectively promoted apoptosis of ARID1A-mutated cells. HDAC6 directly deacetylated the Lysine 120 residue of p53, a pro-apoptotic post-translational modification. Thus, ARID1A mutation inactivates p53’ apoptotic function by upregulating HDAC6. These results indicate that pharmacological inhibition of HDAC6 is a novel therapeutic strategy involving ARID1A-mutation

2017-07-14 | GSE84405 | GEO

MAP3K4 Kinase Activity Controls Chromatin Remodelers for Transitions Between Epithelial and Mesenchymal Phenotypes in Trophoblast Stem Cells [RNA-Seq]

Project description:MAP3K4 is a serine/threonine kinase that regulates epithelial to mesenchymal transition (EMT). Trophoblast stem (TS) cells lacking MAP3K4 kinase activity (TSKI4 cells) are in an intermediate state of EMT, having reduced epithelial and increased mesenchymal marker expression. Reduced epithelial gene expression in TSKI4 cells was due to loss of H2BK5 promoter acetylation catalyzed by the histone acetyltransferase CBP. Herein, we show that MAP3K4 also regulates the ubiquitination and degradation of the deacetylase HDAC6. Due to the loss of MAP3K4 kinase activity, TSKI4 cells have elevated HDAC6 expression and activity. Knockdown of HDAC6 in TSKI4 cells restores epithelial features, defining HDAC6 as a key regulator of EMT controlled by MAP3K4. HDAC6 promotes EMT by directly deacetylating H2BK5 on promoters of tight junction genes claudin6 and occludin, inhibiting their expression. Thus, MAP3K4 is a master regulator that coordinates chromatin modifiers, CBP and HDAC6, to regulate the transition between epithelial and mesenchymal states.

2017-03-07 | GSE92425 | GEO

MAP3K4 Kinase Activity Controls Chromatin Remodelers for Transitions Between Epithelial and Mesenchymal Phenotypes in Trophoblast Stem Cells [ChIP-Seq]

2017-03-07 | GSE92394 | GEO

CTCF acetylation at lysine 20 is required for the early cardiac mesoderm differentiation of embryonic stem cells.

Project description:The CCCTC-binding factor (CTCF) protein and its modified forms regulate gene expression and genome organization. However, information on CTCF acetylation and its biological function is still lacking. Here, we show that CTCF can be acetylated at lysine 20 (CTCF-K20) by CREB-binding protein (CBP) and deacetylated by histone deacetylase 6 (HDAC6). CTCF-K20 is required for the CTCF interaction with CBP. A CTCF point mutation at lysine 20 had no effect on self-renewal but blocked the mesoderm differentiation of mouse embryonic stem cells (mESCs). The CTCF-K20 mutation reduced CTCF binding to the promoters and enhancers of genes associated with early cardiac mesoderm differentiation, resulting in diminished chromatin accessibility and decreased enhancer-promoter interactions, impairing gene expression. In summary, this study reveals the important roles of CTCF-K20 in regulating CTCF genomic functions and mESC differentiation into mesoderm.

| S-EPMC9482892 | biostudies-literature

A complex containing lysine-acetylated actin inhibits the formin INF2

Project description:INF2 is a member of the formin family of actin assembly factors. Dominant mis-sense mutations in INF2 link to two diseases: focal segmental glomerulosclerosis (FSGS), a kidney disease; and Charcot-Marie-Tooth disease (CMTD), a neuropathy. All disease mutations map to the autoinhibitory Diaphanous Inhibitory Domain (DID). Curiously, purified INF2 is not autoinhibited, suggesting the existence of additional cellular inhibitors. We purified an INF2 inhibitor from mouse brain, and identified it as a complex between lysine-acetylated actin (KAc-actin) and cyclase-associated protein (CAP). Inhibition of INF2 by CAP/KAc-actin requires INF2 DID. Treatment of CAP/KAc-actin with histone deacetylase 6 (HDAC6) releases INF2 inhibition, while HDAC6 inhibitors block cellular INF2 activation. INF2 disease mutants are poorly inhibited by CAP/KAc-actin, suggesting that FSGS and CMTD result from reduced CAP/KAc-actin binding. This is the first demonstrated role for lysine-acetylated actin: regulation of an actin assembly factor by a novel mechanism, which we call facilitated auto-inhibition.

2018-07-18 | MSV000082634 | MassIVE

Coordination of Rel Expression by MAP3K4, CBP, and HDAC6 Controls TS cell Phenotype (RNA-seq)

Project description:Trophoblast stem cells lack MAP3K4 activity (TSKI4 cells) switch from epithelial phenotype to intermediate phenotype. Loss of epithelial phenotype is due to the loss of CBP histone acetyltransferase activity and the gain of histone deacetylase HDAC6 expression and activity. In our work, we identify a small network of 183 genes whose expression is co-regulated by MAP3K4, CBP, and HDAC6. Further, we define the key role of one of these co-regulated genes, Rel, in inducing epithelial phenotype in intermediate TSKI4 cells.

2020-08-28 | GSE148496 | GEO

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