Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DOT1L inhibition reveals a distinct class of enhancers dependent upon H3K79 methylation

ABSTRACT: DOT1L inhibition reveals a distinct class of enhancers dependent upon H3K79 methylation

PROVIDER: PRJNA483451 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7620640_1.fastq.gz	Fastqsanger.gz
	SRR7620640_2.fastq.gz	Fastqsanger.gz
	SRR7620800_1.fastq.gz	Fastqsanger.gz
	SRR7620800_2.fastq.gz	Fastqsanger.gz
	SRR7620810_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 125

Similar Datasets

DOT1L-controlled cell-fate determination and transcription elongation are independent of H3K79 methylation

Project description:Actively transcribed genes in mammals are decorated by H3K79 methylation, which is correlated with transcription levels and is catalyzed by the histone methyltransferase DOT1L. DOT1L is required for mammalian development, and the inhibition of its catalytic activity has been extensively studied for cancer therapy; however, the mechanisms underlying DOT1L’s functions in normal development and cancer pathogenesis remain elusive. To dissect the relationship between H3K79 methylation, cellular differentiation, and transcription regulation, we systematically examined the role of DOT1L and its catalytic activity in embryonic stem cells (ESCs). DOT1L is dispensable for ESC self-renewal but is required for establishing the proper expression signature of neural progenitor cells, while catalytic inactivation of DOT1L has a lesser effect. Furthermore, DOT1L loss, rather than its catalytic inactivation, causes defects in glial cell specification. Although DOT1L loss by itself has no major defect in transcription elongation, transcription elongation defects seen with the super elongation complex inhibitor KL-2 are exacerbated in DOT1L knockout cells, but not in catalytically dead DOT1L cells, revealing a role of DOT1L in promoting productive transcription elongation that is independent of H3K79 methylation. Taken together, our study reveals a catalytic-independent role of DOT1L in modulating cell-fate determination and in transcriptional elongation control.

2020-10-21 | GSE134083 | GEO

AF9 Links Histone Acetylation to DOT1L-Mediated H3K79 Methylation

Project description:The recognition of modified histones by “reader” proteins constitutes a key mechanism regulating gene expression in the chromatin context. Compared with the great variety of readers for histone methylation, few protein modules that recognize histone acetylation are known. Here we show that the evolutionarily conserved YEATS domains constitute a novel family of acetyllysine readers. The human AF9 YEATS domain binds strongly to histone H3K9 acetylation and, to a lesser extent, H3K27 and H3K18 acetylation. Crystal structural studies revealed that AF9 YEATS adopts an eight-stranded immunoglobin fold and utilizes a serine-lined aromatic “sandwiching” cage for acetyllysine readout, representing a novel recognition mechanism that is distinct from that of known acetyllysine readers. Histone acetylation recognition by AF9 is important for the chromatin recruitment of the H3K79 methyltransferase DOT1L. Together, our studies identify the YEATS domain as a novel acetyllysine-binding module, thereby establishing the first direct link between histone acetylation and DOTL1-mediated H3K79 methylation in transcription control. ChIP-seq analysis of AF9, H3K79me3, H3K9ac in Hela cells and H3K79me3 in Hela AF9 knockdown and Hela Dot1L knockdown cells.

2014-12-11 | E-GEOD-60366 | biostudies-arrayexpress

DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation (Capture-C)

Project description:DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation (Capture-C)

| PRJNA483454 | ENA

DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation (ATAC-seq)

Project description:DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation (ATAC-seq)

| PRJNA483453 | ENA

DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation (ChIP-seq)

Project description:DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation (ChIP-seq)

| PRJNA483455 | ENA

DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation (RNA-seq)

Project description:DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation (RNA-seq)

| PRJNA528308 | ENA

H3K79me2 ChIP-seq in cerebellar granular neurons (CGN) and progenitors (CGNP) upon DOT1L inhibition with SGC0946 in vitro

Project description:DOT1L as methyltransferase of H3K79 is implicated in brian development. Here, we further defined DOT1L function within the granular neurons during cerebellar development using ChIP-seq of H3K79 dimethylation of isolated cerebellar granular neurons and progenitors. Thereby we compared samples treated with a DOT1L inhibitor versus DMSO treated cells. The data sets reveals new important targets of DOT1L, which ensure a correct development of the cerebellum.

2018-10-15 | GSE101947 | GEO

DOT1L Inhibits SIRT1 and SUV39H1-Mediated H3K9 Modification to Maintain Gene Expression (array)

Project description:Methylation of histone 3 on lysine 79 (H3K79) is broadly associated with active gene expression in eukaryotes, and the H3K79 methyltransferase DOT1L is indispensable for specific leukemia subtypes like those with MLL-translocations. We found that suppression of the histone deacetylase SIRT1 rescued MLL-AF9 leukemia cells from their dependence on DOT1L. We show that upon DOT1L inhibition, SIRT1 is required for the acquisition of a repressive chromatin state consistent with facultative heterochromatin around MLL-AF9 target genes in leukemia and other genes possess an H3K79me2(hi), H3K9ac(hi), H3K9me2(low) histone modification profile in normal hematopoietic stem and progenitor cells. Examination of gene expression dynamics with and without drug treatment and RNA interference.

2015-03-30 | E-GEOD-61013 | biostudies-arrayexpress

DOT1L Inhibits SIRT1 and SUV39H1-Mediated H3K9 Modification to Maintain Gene Expression (ATACseq)

Project description:Methylation of histone 3 on lysine 79 (H3K79) is broadly associated with active gene expression in eukaryotes, and the H3K79 methyltransferase DOT1L is indispensable for specific leukemia subtypes like those with MLL-translocations. We found that suppression of the histone deacetylase SIRT1 rescued MLL-AF9 leukemia cells from their dependence on DOT1L. We show that upon DOT1L inhibition, SIRT1 is required for the acquisition of a repressive chromatin state consistent with facultative heterochromatin around MLL-AF9 target genes in leukemia and other genes possess an H3K79me2(hi), H3K9ac(hi), H3K9me2(low) histone modification profile in normal hematopoietic stem and progenitor cells. Examination of histone modifications and a chromatin modifier with and without drug treatment and RNA interference.

2015-03-30 | E-GEOD-61016 | biostudies-arrayexpress

DOT1L Inhibits SIRT1 and SUV39H1-Mediated H3K9 Modification to Maintain Gene Expression (ChIPseq)

Project description:Methylation of histone 3 on lysine 79 (H3K79) is broadly associated with active gene expression in eukaryotes, and the H3K79 methyltransferase DOT1L is indispensable for specific leukemia subtypes like those with MLL-translocations. We found that suppression of the histone deacetylase SIRT1 rescued MLL-AF9 leukemia cells from their dependence on DOT1L. We show that upon DOT1L inhibition, SIRT1 is required for the acquisition of a repressive chromatin state consistent with facultative heterochromatin around MLL-AF9 target genes in leukemia and other genes possess an H3K79me2(hi), H3K9ac(hi), H3K9me2(low) histone modification profile in normal hematopoietic stem and progenitor cells. Examination of histone modifications and a chromatin modifier with and without drug treatment and RNA interference.

2015-03-30 | E-GEOD-61021 | biostudies-arrayexpress

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