Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [PBAT]

ABSTRACT: Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [PBAT]

PROVIDER: PRJNA705713 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13817151_1.fastq.gz	Fastqsanger.gz
	SRR13817151_2.fastq.gz	Fastqsanger.gz
	SRR13817152_1.fastq.gz	Fastqsanger.gz
	SRR13817152_2.fastq.gz	Fastqsanger.gz
	SRR13817153_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [PBAT]

Project description:Histone 3 lysine 4 trimethylation (H3K4me3) is an epigenetic mark found at active gene promoters and CpG islands. H3K4me3 is essential for mammalian development, yet mechanisms underlying its genomic targeting are poorly understood. H3K4me3 methyltransferases SETD1B and MLL2 are essential for oogenesis. We investigated changes in H3K4me3 in Setd1b conditional knockout (cKO) GV oocytes using ultra-low input ChIP-seq, in complement to DNA methylation and gene expression analysis. Setd1b cKO oocytes showed a redistribution of H3K4me3, with a marked loss at active gene promoters associated with downregulated gene expression. Remarkably, many regions gained H3K4me3 in Setd1b cKOs, in particular those that were DNA hypomethylated, transcriptionally inactive and CpG-rich. All of these are hallmarks of MLL2 targets; thus, loss of SETD1B appears to enable enhanced MLL2 activity. Our work reveals two distinct, complementary mechanisms of genomic targeting of H3K4me3 in oogenesis, with SETD1B linked to transcriptional activity and MLL2 to CpG content.

2022-01-17 | GSE167986 | GEO

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [ChIP-seq]

2022-01-17 | GSE167985 | GEO

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [RNA-seq]

2022-01-17 | GSE167984 | GEO

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte

Project description:Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte

| PRJNA705707 | ENA

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [RNA-seq]

Project description:Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [RNA-seq]

| PRJNA705709 | ENA

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [ChIP-seq]

Project description:Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [ChIP-seq]

| PRJNA705711 | ENA

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte

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

2022-01-17 | GSE167987 | GEO

The histone 3 lysine 4 methyltransferase Setd1b is a maternal effect gene required for the oogenic gene expression program

Project description:Germ cell development involves major reprogramming of the epigenome to prime the zygote for totipotency. Histone 3 lysine 4 (H3K4) methylations are universal epigenetic marks mediated in mammals by six H3K4 methyltransferases related to fly Trithorax, including two yeast Set1 orthologs: Setd1a and Setd1b. Whereas Setd1a plays no role in oogenesis, we report that Setd1b deficiency causes female sterility. Oocyte specific Gdf9iCre conditional knockout (Setd1bGdf9cKO) ovaries develop through all stages however follicular loss accumulated with age and unfertilized metaphase II (MII) oocytes exhibited irregularities of the zona pellucida and meiotic spindle. Most Setd1bGdf9cKO zygotes remained in the pronuclear stage and displayed polyspermy in the perivitelline space. Expression profiling of Setd1bGdf9cKO MII oocytes revealed (i) that Setd1b promotes the expression of the major oocyte transcription factors including Obox1, 2, 5, 7, Meis2 and Sall4; and (ii) two-times more up- than downregulated mRNAs suggesting that Setd1b also promotes the expression of negative regulators of oocyte development with multiple Zfp-KRAB factors implicated. Together, these findings indicate that Setd1b serves as maternal effect gene through regulation of the oocyte gene expression program.

2017-02-09 | GSE85360 | GEO

Comparative gene expression analysis in OCI-LY19 isogenic cell lines with SETD1B mutation or KMT2D+SETD1B double mutants.

Project description:The translocation t(14;18) activates BCL2 and is considered the initiating genetic lesion in most follicular lymphomas (FL). Surprisingly, FL patients fail to respond to the BCL2 inhibitor, Venetoclax. We show that mutations and deletions affecting the histone lysine methyltransferase SETD1B (KMT2G) occur in 7% of FLs and in 16% of diffuse large B cell lymphomas (DLBCL). Deficiency in SETD1B confers striking resistance to Venetoclaxand to an experimental MCL-1 inhibitor. SETD1B also acts as a tumor suppressor andcooperates with loss ofKMT2Din lymphoma development in vivo. Consistently, loss of SETD1B in human lymphomas typically coincides with loss of KMT2D. Mechanistically, SETD1B is required for the expression of several pro-apoptotic BCL2 family proteins. Conversely, inhibitors of the KDM5 histoneH3K4demethylases restore BIM and BIK expression and synergize with Venetoclax inSETD1B-deficient lymphomas.

2024-08-23 | GSE273152 | GEO

H3K5me3 modifications in OCI-LY19 cells with and without SETD1B mutations.

2024-08-23 | GSE273154 | GEO