Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genetic dissection of gene silencing mediated by H3K27 methylation

ABSTRACT: Genetic dissection of gene silencing mediated by H3K27 methylation

PROVIDER: PRJNA542356 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9041320.fastq.gz	Fastqsanger.gz
	SRR9041330.fastq.gz	Fastqsanger.gz
	SRR9041340.fastq.gz	Fastqsanger.gz
	SRR9041350.fastq.gz	Fastqsanger.gz
	SRR9041360.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 68

Similar Datasets

Genetic dissection of gene silencing mediated by H3K27 methylation

Project description:We are intereted in changes in transcriptome in putative polycomb mutants generated by exposure to UV light. We included polycomb mutants made by reverse genetics and other WT strains with different genetic backgrounds used as parents for bulk segregant analysis.

2020-01-01 | GSE131036 | GEO

Gene expression and H3K27 tri-methylation analysis of meristematic tissue (Me) and young leaves (Le) isolated by manual dissection of clv3-9 plants

Project description:This SuperSeries is composed of the following subset Series: GSE24464: Expression analysis of meristematic tissue (Me) and young leaves (Le) isolated by manual dissection of clv3-9 plants GSE24474: H3K27 tri-methylation analysis of meristematic tissue (Me) and young leaves (Le) isolated by manual dissection of clv3-9 plants Refer to individual Series

2011-04-20 | E-GEOD-24507 | biostudies-arrayexpress

Genetic dissection of the Fgf5 enhancer cluster

Project description:Genetic dissection of the Fgf5 enhancer cluster

| PRJEB37478 | ENA

H3K36 methylation antagonizes PRC2-mediated H3K27 methylation.

Project description: Not available

| S-EPMC3048685 | biostudies-literature

Genetic dissection of the α-globin super-enhancer

Project description:Genetic dissection of the α-globin super-enhancer

| PRJNA314091 | ENA

Loss of H3K27 monomethylation leads to DNA-methylation-independent release of gene silencing

Project description:Constitutive heterochromatin in Arabidopsis thaliana is marked by repressive chromatin modifications including DNA methylation, histone 3 dimethylation at lysine 9 (H3K9me2), and monomethylation at lysine 27 (H3K27me1). The enzymes catalyzing DNA methylation and H3K9me2 have been identified and mutations in these proteins lead to the reactivation of silenced heterochromatic elements. The enzymes responsible for heterochromatic H3K27me1, in contrast, remain unknown. Here we show that the divergent SET-domain proteins ARABIDOPSIS TRITHORAX-RELATED PROTEIN5 (ATXR5) and ATXR6 exhibit H3K27 monomethyltransferase activity and double mutants have reduced H3K27me1 in vivo and show partial heterochromatin decondensation. atxr5 atxr6 plants also show transcriptional activation of repressed heterochromatic elements. Interestingly, H3K9me2 and DNA methylation are unaffected in the double mutant. These results indicate that ATXR5 and ATXR6 form a novel class of H3K27 methyltransferases and that H3K27me1 represents a new pathway required for transcriptional repression in Arabidopsis. Comparison of methylation in wild type and ATXR6/ATXR6 mutants

2009-05-31 | E-GEOD-16071 | biostudies-arrayexpress

Analysis of genes bound by ULK3 and of H3K27 histone modification plus/minus ULK3 silencing in SCC13 cells

Project description:We report high-throughput profiling of genes bound by ULK3 and of H3K27 histone modification plus/minus ULK3 silencing in squamous cell carcinoma SCC13 cells .

2022-10-10 | GSE183933 | GEO

Identification and genetic dissection of convergent persister cell states

Project description:Identification and genetic dissection of convergent persister cell states

| PRJNA954422 | ENA

Loss of H3K27 monomethylation leads to DNA-methylation-independent release of gene silencing

2009-06-01 | GSE16071 | GEO

Accurate H3K27 methylation patterns can be established de novo by SUZ12-directed PRC2

Project description:The Polycomb repressive complex 2 (PRC2) catalyzes H3K27 methylation and is required for maintaining transcriptional patterns and cellular identity, but the specification and maintenance of genomic PRC2 binding and H3K27 methylation patterns remain incompletely understood. Epigenetic mechanisms have been proposed, wherein pre-existing H3K27 methylation directs recruitment and regulates the catalytic activity of PRC2 to support its own maintenance. Here we investigate if such mechanisms are required for specifying H3K27 methylation patterns in mouse embryonic stem cells. Through genetic knockouts of subunits, we find that PRC2 is responsible for all levels of H3K27 methylation, and that methylation patterns can be accurately established de novo, when a subunit is reintroduced in the absence of pre-existing H3K27 methylation and PRC2 chromatin binding. Furthermore, we find that the core-subunit SUZ12 directs genomic binding of PRC2, which is essential for establishing correct methylation patterns.

2018-01-12 | GSE103685 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data