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Phase separation of phospho-HDAC6 drives aberrant chromatin architecture in triple-negative breast cancer [Hi-C]

ABSTRACT: Phase separation of phospho-HDAC6 drives aberrant chromatin architecture in triple-negative breast cancer [Hi-C]

PROVIDER: PRJNA1069026 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27729307_1.fastq.gz	Fastqsanger.gz
	SRR27729307_2.fastq.gz	Fastqsanger.gz
	SRR27729308_1.fastq.gz	Fastqsanger.gz
	SRR27729308_2.fastq.gz	Fastqsanger.gz
	SRR27729309_1.fastq.gz	Fastqsanger.gz

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Phase separation of phospho-HDAC6 drives aberrant chromatin architecture in triple-negative breast cancer [Hi-C]

Project description:To investigate the Nexturastat A effects on chromatin structure which disrupt phospho-HDAC6 LLPS in triple-negative breast cancer (TNBC), we conducted the analysis of Hi-C in TNBC cells treated with or without Nexturastat A.

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Phase separation of phospho-HDAC6 drives aberrant chromatin architecture in triple-negative breast cancer [RNA-seq]

Project description:To further elucidate the role of phospho-HDAC6 LLPS in transcriptional regulation, we performed RNA-seq experiments in TNBC cells treated with Nexturastat A or HDAC6 knockdown

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Phase separation of phospho-HDAC6 drives aberrant chromatin architecture in triple-negative breast cancer [ChIP-seq, Cut&Tag, ATAC-seq]

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Phase separation of phospho-HDAC6 drives aberrant chromatin architecture in triple-negative breast cancer [RNA-seq]

Project description:Phase separation of phospho-HDAC6 drives aberrant chromatin architecture in triple-negative breast cancer [RNA-seq]

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Phase separation of phospho-HDAC6 drives aberrant chromatin architecture in triple-negative breast cancer [ChIP-seq, Cut&Tag, ATAC-seq]

Project description:Phase separation of phospho-HDAC6 drives aberrant chromatin architecture in triple-negative breast cancer [ChIP-seq, Cut&Tag, ATAC-seq]

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Aberrant phase separation of transcription factors in human developmental disorders

Project description:Components of the transcription machinery can undergo liquid-liquid phase separation, but the functional importance of phase-separated condensates in transcriptional control is not well understood. Here we report that disease-causing mutations in several transcription factors (TFs) alter the phase separation capacity of those TFs. We first demonstrate that the Hoxd13 TF, and its intrinsically disordered N-terminus form phase-separated condensates. Expansions of a polyalanine repeat, which cause hereditary synpolydactyly in humans, facilitate phase separation of Hoxd13, and alter the transcriptional program of several cell types in a cell-specific manner in vivo. Disease-associated expansions of aminoacid repeats in intrinsically disordered regions of other TFs were similarly found to alter phase separation. These results suggest that aberrant phase separation of transcriptional regulators may underlie a spectrum of human pathologies. The paper is available at https://doi.org/10.1016/j.cell.2020.04.018

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Aberrant phase separation of transcription factors in human developmental disorders

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Seizure-induced LIN28A disrupts pattern separation via aberrant hippocampal neurogenesis

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Hdac6 regulates Tip60-p400 function in stem cells (sequencing)

Project description:The Tip60 (also known as Kat5) lysine acetyltransferase functions broadly as a transcriptional co-activator that acetylates histones. In contrast, Tip60 functions in embryonic stem cells (ESCs) both to silence genes that promote differentiation and to activate genes required for proliferation. The mechanism by which Tip60 functions as a repressor is unknown. Here we show that the class II histone deacetylase Hdac6 co-purifies with Tip60-p400 complex from ESCs and is necessary for complete silencing of most differentiation genes targeted by Tip60. In contrast to differentiated cells, where Hdac6 is mainly cytoplasmic and does not interact with Tip60, Hdac6 is largely nuclear in ESCs and neural stem cells (NSCs) and interacts with Tip60-p400 in both cell types. Hdac6 is enriched at promoters bound by Tip60-p400 in ESCs, but while Tip60 binds on both sides of transcription start sites (TSSs), Hdac6 binding overlaps with only the downstream Tip60 peak. Surprisingly, Hdac6 does not deacetylate histones at these sites, but rather is required for Tip60 binding. These data suggest that nuclear exclusion of Hdac6 during differentiation plays a major role in modulation of Tip60-p400 function. We determined the genome-wide localization of Tip60 and Hdac6 in mouse ES cells, and examined genomic binding profiles of Tip60 and Hdac6 upon indicated knockdown by ChIP-seq. We examined genomic binding profiles of p400 upon indicated knockdown by ChIP-seq.

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HDAC6 Inhibition Disrupts HDAC6-P300 Interaction Reshaping the Cancer Chromatin Landscape (ChIP-Seq)

Project description:Histone deacetylases (HDACs) are crucial regulators of gene expression, DNA synthesis, and cellular processes, making them essential targets in cancer research. HDAC6, specifically, influences protein stability and chromatin dynamics. Despite HDAC6's potential therapeutic value, its exact role in gene regulation and chromatin remodeling needs further clarification. This study examines how HDAC6 inactivation influences lysine acetyltransferase P300 stabilization and subsequent effects on chromatin structure and function in cancer cells. We employed the HDAC6 inhibitor ITF3756, siRNA, or CRISPR/Cas9 gene editing to inactivate HDAC6 in different epigenomic backgrounds. Constantly, this inactivation led to significant changes in chromatin accessibility, particularly increased acetylation of histone H3 lysines 9, 14, and 27 (ATAC-seq and H3K27Ac ChIP-seq analysis). Transcriptomics, proteomics, and gene ontology analysis revealed gene changes in cell proliferation, adhesion, migration, and apoptosis. Significantly, HDAC6 inactivation altered P300 ubiquitination, stabilizing P300 and leading to downregulating genes critical for cancer cell survival. Our study highlights the substantial impact of HDAC6 inactivation on the chromatin landscape of cancer cells and suggests a role for P300 in contributing to the anticancer effects. The stabilization of P300 with HDAC6 inhibition proposes a potential shift in therapeutic focus from HDAC6 itself to its interaction with P300. This finding opens new avenues for developing targeted cancer therapies, improving our understanding of epigenetic mechanisms in cancer cells.

2024-08-19 | GSE273645 | GEO

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