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Genome-wide maps of chromatin state for histone modifications and chromatin remodeling factors in WT and PHF6-KO conditions in Jurkat T-ALL cells.

ABSTRACT: Genome-wide maps of chromatin state for histone modifications and chromatin remodeling factors in WT and PHF6-KO conditions in Jurkat T-ALL cells.

PROVIDER: PRJNA797372 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17665646_1.fastq.gz	Fastqsanger.gz
	SRR17665646_2.fastq.gz	Fastqsanger.gz
	SRR17665647_1.fastq.gz	Fastqsanger.gz
	SRR17665647_2.fastq.gz	Fastqsanger.gz
	SRR17665648_1.fastq.gz	Fastqsanger.gz

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Genome-wide maps of chromatin state for histone modifications and chromatin remodeling factors in WT and PHF6-KO conditions in Jurkat T-ALL cells.

Project description:We have carried out high-throughput profiling of histone modifications and transcription factors in mammalian cells. First we generated stable PHF6 knock out lines by CRISPR-Cas9 technology in wild type Jurkat cells. We electroporated the RNP complex in Jurkat cells conatining guide RNAs against either non-targeting (EV) or PHF6 (KO) followed by single clone isolation and expansion. We confirmed absolute loss of total protein by WB and indel formation (mutation efficiency) at the PHF6 genomic locus by Sanger sequencing. By obtaining over six to ten billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of well studied histone modifications and transcription factors. This study provides a framework for eluciadting the role of PHF6 in regulating the chromatin landscape encompassing both activating and repressive histone modifications and chromatin remodelers in the context of leukemia.

2025-01-13 | GSE193713 | GEO

PHF6 keeps hematopoietic lineage development in check [Jurkat]

Project description:Analysis of the mutational landscape of various hematological malignancies has shown that key regulators implicated in lineage commitment and differentiation are frequently implicated in leukemic transformation. In T-cell acute lymphoblastic leukemia, the role of various oncogenic and tumor suppressing transcription factors has been investigated. More recently, an exceptional high prevalence of mutations affecting epigenetic modifiers in T-ALL has also been noted. In order to understand the exact contribution of such lesions to normal differentiation and oncogenic transformation, further functional characterization of this subclass of proteins is warranted. PHF6 is one of these key epigenetic players, which was described as a frequently mutated and deleted novel tumor suppressor in T-ALL. In a first step towards unraveling the role of PHF6 in normal and malignant hematopoiesis, we characterized the function of PHF6 in both normal T-cell differentiation and other hematopoietic lineages as a prelude to understand its contribution to leukemogenesis. Here, we show for the first time that PHF6 controlled epigenetic regulation positively controls a NOTCH1 gene signature and the effects observed on T-lineage differentiation seem to be additive with Notch1. In this study, we show for the first time that PHF6 is a master regulator of early hematopoietic differentiation along the T-cell, B-cell, myeloid and NK-cell lineages.

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Chromatin accessibility changes caused by PHF6 knockout in THP1 human AML cell line

Project description:PHF6 is a transcriptional regulator mutated in 3-5% of acute myeloid leukemia. To understand how PHF6 and its functional partner PHIP interact with each other on chromatin, we performed ChIP-Seq for PHF6 (in the presence and absence of PHIP), and for PHIP. We observd that PHF6 and PHIP peaks overlap on chromatin, and PHF6 requires PHIP for its chromatin occupancy. ATAC-Seq and H3K27ac ChIP-Seq showed that PHF6 and PHIP occupy open and active regions of the genome.

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PHF6 OCCUPANCYIN HUMAN T-CELL ACUTE LYMPHOBLASTIC LEUKEMIA

Project description:Here we identify the genome-wide occupancy of PHF6 in T-ALL cells. Human T-ALL cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total PHF6 (Bethyl A301-451A). This represents the ChIP-seq portion of this dataset.

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PHF6 drives satellite DNA chromatin remodeling for resolution of replicative stress-induced DNA damage

Project description:The Plant Homeodomain 6 gene (PHF6) encodes a nucleolar and chromatin-associated factor with proposed roles in chromatin remodeling and transcription regulation. Germline mutations in PHF6 are causative of Börjesson-Forsmann-Lehman syndrome, while somatic loss-of-function genetic alterations support a tumor suppressor role in leukemia. Yet, the specific molecular function and mechanisms of PHF6 remain poorly understood. Here we show that PHF6 associates with chromatin remodeling and DNA repair factors in multiprotein complexes at satellite repeat heterochromatin regions and facilitates double strand break repair in the context of replicative stress-induced DNA damage. Mechanistically, PHF6 localizes to sites of DNA damage and its inactivation impairs the resolution of DNA breaks promoting the accumulation of single and double-stranded DNA lesions. In addition, PHF6 associates with difficult to replicate Histone H3 lysine 9 trimethylation (H3K9me3)-marked heterochromatin at satellite DNA regions, prevents accelerated replication fork dynamics and is required to maintain genomic integrity at fragile sites. In all, these results demonstrate a critical role for PHF6-containing chromatin-remodeling complexes in homologous recombination DNA-repair and in the resolution of satellite DNA-associated replicative stress.

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Project description:PHF6 is a transcriptional regulator mutated in 3-5% of acute myeloid leukemia. To understand how PHF6 and its functional partner PHIP interact with each other on chromatin, we performed ChIP-Seq for PHF6 (in the presence and absence of PHIP), for PHF6R274Q mutant, and for PHIP. We observd that PHF6 and PHIP peaks overlap on chromatin, and PHF6 requires PHIP for its chromatin occupancy. ATAC-Seq and H3K27ac ChIP-Seq showed that PHF6 and PHIP occupy open and active regions of the genome.

2024-11-15 | GSE281627 | GEO

Genome-wide maps of chromatin modifications in wild-type or mutant HAP1 cells

Project description:Genome-wide maps of chromatin modifications in wild-type or mutant HAP1 cells

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PHF6 occupancy in THP1 human AML cell line in wildtype, PHF6R274Q mutant, and PHIP knockout cells

Project description:PHF6 is a transcriptional regulator mutated in 3-5% of acute myeloid leukemia. To understand how PHF6 and its functional partner PHIP interact with each other on chromatin, we performed ChIP-Seq for PHF6 (in the presence and absence of PHIP), for PHF6R274Q mutant, and for PHIP. We observd that PHF6 and PHIP peaks overlap on chromatin, and PHF6 requires PHIP for its chromatin occupancy. ATAC-Seq and H3K27ac ChIP-Seq showed that PHF6 and PHIP occupy open and active regions of the genome.

2024-11-15 | GSE281628 | GEO

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