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Changes in H3K27 acetylation in THP1 human AML cell line on PHF6 knockout, PHF6R274Q mutation, PHIP knockout, and double knockout of PHF6 and PHIP compared to wildtype clones

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE281627 | GEO | 2024/11/15

REPOSITORIES: GEO

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			Action	DRS
		Other
	GSE281627_DKO_THP1_H3K27ac-ChIP_Rep1.bw	Other
	GSE281627_DKO_THP1_H3K27ac-ChIP_Rep2.bw	Other
	GSE281627_DKO_THP1_H3K27ac-ChIP_Rep3.bw	Other
	GSE281627_PHF6KO_THP1_H3K27ac-ChIP_Rep1.bw	Other

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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

Transcriptomic changes in THP1 human AML cell line on PHF6 knockout, PHF6R274Q mutation, PHIP knockout, and double knockout of PHF6 and PHIP compared to wildtype cells

Project description:PHF6 is a transcriptional regulator mutated in 3-5% of acute myeloid leukemia. To understand the effect of loss and clinical mutation of PHF6 on the transcriptome of myeloid cells, we generated multiple wildtype and PHF6 knockout clones, as well as clones expressing the most common clinical mutant of the protein-PHF6R274Q. We observed that both single and double knockouts and mutation of PHF6 shifted the cells towards stemness and away from differentiation. Additionally we identified PHIP as a possible functional partner for PHF6. To investigate their common biological function, we generated multiple single knockout clones of PHIP as well as double knockout clones of PHIP and PHF6, and observed that, similar to single knockout of PHF6, PHIP knockout and double knockout also shifted cells towards stemness and away from differentiation. Collectively, our experiments show that PHF6 and PHIP, separately identified as being mutated in AML, exert similar downstream effects on the AML transcriptome.

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Transcriptomic changes in PHF6 knockout THP1 human AML cell line on rescue with PHF6 wildtype (with and without PHIP) or rescue with PHF6R274Q mutant

2024-11-15 | GSE281624 | GEO

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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Project description:CRISPR Cas9 guided knockout (KO) of PHF6 in human THP1 AML cell line. We performed bulk RNA-Seq on knockout (PHF6 KO) and wildtype (CTRL) clones derived from THP1 cells transduced with lentiviral vectors encoding Cas9 protein and either PHF6 gRNAs or non-targeting gRNAs. Our results reveal that PHF6 knockout upregulates self-renewal gene sets and downregulates myeloid differentiation gene sets.

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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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