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Dual interactions of K27M mutant nucleosomes with PRC2 and MLL1 shape the cancer epigenetic landscape (ATAC-seq)

ABSTRACT: Dual interactions of K27M mutant nucleosomes with PRC2 and MLL1 shape the cancer epigenetic landscape (ATAC-seq)

PROVIDER: PRJNA685160 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13252800_1.fastq.gz	Fastqsanger.gz
	SRR13252800_2.fastq.gz	Fastqsanger.gz
	SRR13252801_1.fastq.gz	Fastqsanger.gz
	SRR13252801_2.fastq.gz	Fastqsanger.gz
	SRR13252802_1.fastq.gz	Fastqsanger.gz

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Dual interactions of K27M mutant nucleosomes with PRC2 and MLL1 shape the cancer epigenetic landscape (ATAC-seq)

Project description:Cancer associated mutations in genes encoding histones dramatically reshape chromatin patterns and support tumorigenesis, despite their low prevalence. Lysine to Methionine substitution of residue 27 on histone H3 (K27M) is a driver mutation in high-grade pediatric gliomas, known to abrogate Polycomb activity. We applied single-molecule systems to image individual nucleosomes and delineate the combinatorial chromatin patterns associated with K27M expression. We find that K27M-mutant nucleosomes not only sequester PRC2, but also bind preferentially to MLL1, thus leading to genome-wide redistribution of H3K4me3. K27M-mediated deregulation of both repressive and activating chromatin marks maintains ‘bivalent’ chromatin, supporting a poorly differentiated cellular state. This study provides evidence for widespread effects of the K27M oncohistone on multiple core epigenetic pathways, and highlights the use of single-molecule tools to reveal mechanisms of chromatin deregulation in cacner.

2022-05-15 | GSE163182 | GEO

Dual interactions of K27M mutant nucleosomes with PRC2 and MLL1 shape the cancer epigenetic landscape (Cut&Run)

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Dual interactions of K27M mutant nucleosomes with PRC2 and MLL1 shape the cancer epigenetic landscape (MARS-seq)

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Dual interactions of K27M mutant nucleosomes with PRC2 and MLL1 shape the cancer epigenetic landscape [CUT&RUN, HEK293]

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Dual interactions of K27M mutant nucleosomes with PRC2 and MLL1 shape the cancer epigenetic landscape

Project description:Dual interactions of K27M mutant nucleosomes with PRC2 and MLL1 shape the cancer epigenetic landscape

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Dual interactions of K27M mutant nucleosomes with PRC2 and MLL1 shape the cancer epigenetic landscape (MARS-seq)

Project description:Dual interactions of K27M mutant nucleosomes with PRC2 and MLL1 shape the cancer epigenetic landscape (MARS-seq)

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Dual interactions of K27M mutant nucleosomes with PRC2 and MLL1 shape the cancer epigenetic landscape (Cut&Run)

Project description:Dual interactions of K27M mutant nucleosomes with PRC2 and MLL1 shape the cancer epigenetic landscape (Cut&Run)

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Dual interactions of K27M mutant nucleosomes with PRC2 and MLL1 shape the cancer epigenetic landscape [CUT&RUN, HEK293]

Project description:Dual interactions of K27M mutant nucleosomes with PRC2 and MLL1 shape the cancer epigenetic landscape [CUT&RUN, HEK293]

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H3 K27M and EZHIP impede H3K27-methylation spreading by inhibing allosterically stimulated PRC2 [K27M]

Project description:In this study, we report that EZHIP and H3 K27M preferentially interact with an allosterically activated form of PRC2 in vivo. The formation of H3 K27M- and EZHIP-PRC2 complexes occurs at CpG islands containing H3K27me3 and impedes PRC2 and H3K27me3 spreading. Moreover, we find that H3 K27M inhibits PRC2 in trans and can reduce H3K27me3 levels independent of chromatin incorporation. While EZHIP is not found outside of placental mammals, we find that expression of human EZHIP reduces H3K27me3 in Drosophila melanogaster through a conserved molecular mechanism.

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H3 K27M and EZHIP impede H3K27-methylation spreading by inhibing allosterically stimulated PRC2 [EZHIP]

2020-10-12 | GSE151979 | GEO