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EZHIP constrains Polycomb Repressive Complex 2 activity in germ cells

ABSTRACT: EZHIP constrains Polycomb Repressive Complex 2 activity in germ cells

PROVIDER: PRJNA534322 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8946980_1.fastq.gz	Fastqsanger.gz
	SRR8946980_2.fastq.gz	Fastqsanger.gz
	SRR8946990_1.fastq.gz	Fastqsanger.gz
	SRR8946990_2.fastq.gz	Fastqsanger.gz
	SRR8947000_1.fastq.gz	Fastqsanger.gz

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EZHIP constrains Polycomb Repressive Complex 2 activity in germ cells.

Project description:The Polycomb group of proteins is required for the proper orchestration of gene expression due to its role in maintaining transcriptional silencing. It is composed of several chromatin modifying complexes, including Polycomb Repressive Complex 2 (PRC2), which deposits H3K27me2/3. Here, we report the identification of a cofactor of PRC2, EZHIP (EZH1/2 Inhibitory Protein), expressed predominantly in the gonads. EZHIP limits the enzymatic activity of PRC2 and lessens the interaction between the core complex and its accessory subunits, but does not interfere with PRC2 recruitment to chromatin. Deletion of Ezhip in mice leads to a global increase in H3K27me2/3 deposition both during spermatogenesis and at late stages of oocyte maturation. This does not affect the initial number of follicles but is associated with a reduction of follicles in aging. Our results suggest that mature oocytes Ezhip-/- might not be fully functional and indicate that fertility is strongly impaired in Ezhip-/- females. Altogether, our study uncovers EZHIP as a regulator of chromatin landscape in gametes.

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Project description:The project aimed at identifying the cofactors regulating Polycomb complex PRC2 enzymatic activity in gonads. We used a knock-in mouse model where the enzymatic subunit of PRC2 (either EZH2 or EZH1) is tagged (Flag-tag) to purify PRC2 from mouse adult testis. This experiment revealed the existence of a new cofactor for PRC2 that we called GPIF (AU022751).

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EZHIP constrains Polycomb Repressive Complex 2 activity in germ cells

Project description:This SuperSeries is composed of the SubSeries listed below.

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EZHIP constrains Polycomb Repressive Complex 2 activity in germ cells (RNA-Seq)

Project description:We identified a novel cofactor of PRC2, expressed predominantly in the gonad, that limits PRC2 enzymatic activity by impeding the interaction between the core complex and the accessory subunits.

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Project description:We identified a novel cofactor of PRC2, expresesd predominantly in the gonad, that lmits PRC2 enzymatic activity by impeding the interaction between the core complex and its accessory subunits.

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Project description:Polycomb-repressive complex 2 (PRC2) catalyzes the methylation of histone H3 Lys27 (H3K27) and functions as a critical epigenetic regulator of both stem cell pluripotency and somatic differentiation, but its role in male germ cell development is unknown. Using conditional mutagenesis to remove the core PRC2 subunits EED and SUZ12 during male germ cell development, we identified a requirement for PRC2 in both mitotic and meiotic germ cells. We observed a paucity of mutant spermatogonial stem cells (SSCs), which appears independent of repression of the known cell cycle inhibitors Ink4a/Ink4b/Arf. Moreover, mutant spermatocytes exhibited ectopic expression of somatic lamins and an abnormal distribution of SUN1 proteins on the nuclear envelope. These defects were coincident with abnormal chromosome dynamics, affecting homologous chromosome pairing and synapsis. We observed acquisition of H3K27me3 on stage-specific genes during meiotic progression, indicating a requirement for PRC2 in regulating the meiotic transcriptional program. Together, these data demonstrate that transcriptional repression of soma-specific genes by PRC2 facilitates homeostasis and differentiation during mammalian spermatogenesis. Examination of two different types of histone modifications (H3K27me3 and H3K4me3) in spermatocytes at two different stages of development (P12 and P17) and the DNA binding protein, EED, in spermatocytes at one stage of development, P17. At P12, there was a single replicate of H3K27me3, H3K4me3 and input. At P17, there were two replicates of H3K27me3, H3K4me3 and input and a single replicate for EED.

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