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Repressive H3K36me2 reader during growth mycelia in the Magnaporthe oryzae

ABSTRACT: Repressive H3K36me2 reader during growth mycelia in the Magnaporthe oryzae

PROVIDER: PRJNA1034113 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26621100_1.fastq.gz	Fastqsanger.gz
	SRR26621100_2.fastq.gz	Fastqsanger.gz
	SRR26621101_1.fastq.gz	Fastqsanger.gz
	SRR26621101_2.fastq.gz	Fastqsanger.gz
	SRR26621102_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing of a repressive H3K36me2 reader during growth mycelia in the Magnaporthe oryzae

Project description:Next Generation Sequencing of a repressive H3K36me2 reader during growth mycelia in the Magnaporthe oryzae

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Genome-wide mapping of a repressive H3K36me2 reader during growth mycelia in the Magnaporthe oryzae

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Genome-wide mapping of a repressive H3K36me2 reader during growth mycelia in the Magnaporthe oryzae

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Next Generation Sequencing of a repressive H3K36me2 reader during growth mycelia in the Magnaporthe oryzae

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Repressive H3K36me2 reader during growth mycelia in the Magnaporthe oryzae

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A repressive H3K36me2 reader mediates Polycomb silencing.

Project description:In animals, evolutionarily conserved Polycomb repressive complex 2 (PRC2) catalyzes histone H3 lysine 27 trimethylation (H3K27me3) and PRC1 functions in recruitment and transcriptional repression. However, the mechanisms underlying H3K27me3-mediated stable transcriptional silencing are largely unknown, as PRC1 subunits are poorly characterized in fungi. Here, we report that in the filamentous fungus Magnaporthe oryzae, the N-terminal chromodomain and C-terminal MRG domain of Eaf3 play key roles in facultative heterochromatin formation and transcriptional silencing. Eaf3 physically interacts with Ash1, Eed, and Sin3, encoding an H3K36 methyltransferase, the core subunit of PRC2, and a histone deacetylation co-suppressor, respectively. Eaf3 co-localizes with a set of repressive Ash1-H3K36me2 and H3K27me3 loci and mediates their transcriptional silencing. Furthermore, Eaf3 acts as a histone reader for the repressive H3K36me2 and H3K27me3 marks. Eaf3-occupied regions are associated with increased nucleosome occupancy, contributing to transcriptional silencing in M. oryzae. Together, these findings reveal that Eaf3 is a repressive H3K36me2 reader and plays a vital role in Polycomb gene silencing and the formation of facultative heterochromatin in fungi.

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Project description:The lysine-to-methionine mutation at residue 27 of histone H3 (H3K27M) is a driving mutation in Diffuse Intrinsic Pontine Glioma (DIPG), a highly aggressive form of pediatric brain tumor with no effective treatment and little chance of survival. H3K27M reshapes the epigenome through a global inhibition of PRC2 catalytic activity, displacement of methylation at lysine 27 of histone H3 (H3K27me2/3), and thus promoting oncogenesis of DIPG. As a consequence, a histone modification H3K36me2, antagonistic to H3K27me2/3, is aberrantly elevated. Here, we investigate the role of H3K36me2 in H3K27M-DIPG by tackling its upstream catalyzing enzymes (writers) and downstream binding factors (readers). We determine that NSD1 and NSD2 are the key writers for H3K36me2. Loss of NSD1/2 in H3K27M-DIPG impedes cellular proliferation in vitro and tumorigenesis in vivo, and disrupts tumor-promoting gene expression programs. Further, we demonstrate that LEDGF and HDGF2 are the main readers that mediate the pro-tumorigenic effects downstream of NSD1/2-H3K36me2. Treatment with a chemically modified peptide mimicking endogenous H3K36me2 dislodges LEDGF/HDGF2 from chromatin and specifically inhibits the proliferation of H3K27M-DIPG. Together, our results indicate a functional pathway of NSD1/2-H3K36me2-LEDGF/HDGF2 as an acquired dependency in H3K27M-DIPG and suggest a possibility to target this pathway for therapeutic interventions.

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