Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: The histone H3.3K36M mutation reprograms the epigenome of chondroblastomas

PROVIDER: PRJNA302855 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR2937470_1.fastq.gz	Fastqsanger.gz
	SRR2937470_2.fastq.gz	Fastqsanger.gz
	SRR2937480_1.fastq.gz	Fastqsanger.gz
	SRR2937480_2.fastq.gz	Fastqsanger.gz
	SRR2937490_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 98

Similar Datasets

The chromatic loci of H3.3K36M determine the preferential prevalence of K36M mutation at H3.3 in chondroblastomas

Project description:The histone H3.3K36M mutation, identified in over 90% of chondroblastoma cases, reprograms the H3K36 methylation landscape and gene expression to promote tumorigenesis. However, it’s still unknown how the H3K36M mutation preferentially happens at the histone H3 variant H3.3. Here we report that, H3.3K36M mutation, but not H3.1K36M mutation, promoted increased colony formation and defects in differentiation. The reduction of H3K36 methylation and initiation of new H3K36 methylation sites in chromatin is dependent on the incorporation loci of H3.3K36M and H3.1K36M. Moreover, while both H3.3K36M and H3.1K36M mutation inactivated the enhancers, only H3.3K36M mutation changed the super enhancers associated with genes in general development, depending on the chromatic incorporation loci of H3.3K36M mutant proteins. Together, this study highlights the roles of the chromatic localization of H3.3K36M mutant proteins in the reprograming of epigenome and subsequent induction of tumorigenesis, and sheds light on the molecular mechanisms how H3K36M mutation mainly occurs at histone H3.3 in chondroblastomas.

2019-05-09 | GSE130858 | GEO

H3K36 mutations promote sarcomagenesis through genome-wide remodeling of H3K36 and H3K27 methylation [Ring1b_ChIP]

Project description:The goal of this study is to understand the genome-wide alterations in chromatin landscape induced by a histone mutation (H3.3K36M) derived from chondroblastomas Examination of genome-wide Ring1b distribution in cells expressing H3.3WT and H3.3K36M.

2016-05-13 | E-GEOD-69286 | biostudies-arrayexpress

H3K36 mutations promote sarcomagenesis through genome-wide remodeling of H3K36 and H3K27 methylation [Cbx2_ChIP]

Project description:The goal of this study is to understand the genome-wide alterations in chromatin landscape induced by a histone mutation (H3.3K36M) derived from chondroblastomas Examination of genome-wide Cbx2 distribution in cells expressing H3.3WT and H3.3K36M.

2016-05-13 | E-GEOD-75856 | biostudies-arrayexpress

A histone H3.3K36M mutation in mice causes imbalance of histone modifications and defects in chondrocyte differentiation [ChIP-seq]

Project description:Histone lysine-to-methionine (K-to-M) mutations have been identified as driver mutations in human cancers. Interestingly, these ‘oncohistone’ mutations inhibit the activity of histone methyltransferases, and, therefore, they can potentially be used as versatile tools to investigate the roles of histone modifications. In this study, we created a conditional knock-in mouse line in which a H3.3K36M mutation can be induced in the endogenous H3.3 gene. Since the H3.3K36M mutation has been identified as a causative mutation of human chondroblastoma, we induced this mutation in the chondrocyte lineage in mouse embryonic limbs. We found that H3.3K36M causes global reduction of H3K36me2 and defects in chondrocyte differentiation. Importantly, the reduction of H3K36me2 was accompanied by a collapse of normal H3K27me3 distribution. Furthermore, the changes in H3K27me3, especially the loss of H3K27me3 at gene regulatory elements, were associated with misregulated expression of a set of genes important for limb development including HoxA cluster genes. Thus, taking advantage of the in vivo induction of H3.3K36M mutation, we reveal the importance of a counterbalance between H3K36me2 and H3K27me3 for chondrocyte differentiation and limb development.

2020-11-01 | GSE150351 | GEO

H3K36 mutations promote sarcomagenesis through genome-wide remodeling of H3K36 and H3K27 methylation [ChIP-Rx]

Project description:The goal of this study is to understand the genome-wide alterations in chromatin landscape induced by a histone mutation (H3.3K36M) derived from chondroblastomas

2016-05-13 | GSE69289 | GEO

H3K36 mutations promote sarcomagenesis through genome-wide remodeling of H3K36 and H3K27 methylation [Ring1b_ChIP]

Project description:The goal of this study is to understand the genome-wide alterations in chromatin landscape induced by a histone mutation (H3.3K36M) derived from chondroblastomas

2016-05-13 | GSE69286 | GEO

H3K36 mutations promote sarcomagenesis through genome-wide remodeling of H3K36 and H3K27 methylation [HA-H33-H31_ChIP]

Project description:The goal of this study is to understand the genome-wide alterations in chromatin landscape induced by a histone mutation (H3.3K36M) derived from chondroblastomas

2016-05-13 | GSE75857 | GEO

H3K36 mutations promote sarcomagenesis through genome-wide remodeling of H3K36 and H3K27 methylation [Cbx2_ChIP]

Project description:The goal of this study is to understand the genome-wide alterations in chromatin landscape induced by a histone mutation (H3.3K36M) derived from chondroblastomas

2016-05-13 | GSE75856 | GEO

A histone H3.3K36M mutation in mice causes imbalance of histone modifications and defects in chondrocyte differentiation [RNA-seq]

2020-11-01 | GSE150352 | GEO

The histone H3.3K36M mutation reprograms the epigenome of chondroblastomas

Project description:Over 90% of chondroblastomas contain a heterozygous mutation replacing lysine 36 with methionine (K36M) in the histone H3 variant H3.3. The role of the H3.3K36M mutation in tumorigenesis of this typically benign bone tumor with high recurrence rates is unknown. Here, we show that H3K36 di- and tri-methylation (me2 and me3) levels are reduced globally in chondroblastomas, as well as in chondrocytes stably expressing the H3.3K36M mutation because the H3.3M36 mutation protein inhibits the activity of lysine methyl transferases, MMSET and SetD2. Remarkably, at gene bodies, H3K36me2 increases and H3K36me3 decreases, which correlates with elevated and reduced expression of the underlying genes, respectively. Genes with altered H3K36me2/me3 and gene expression are associated with cancer pathways and chondrocyte differentiation. Chondrocytes harboring the H3.3K36M mutation exhibit cancer-associated cellular phenotypes and delayed chondrocyte differentiation associated with reduced Bmp2 and Runx2 expression. Exogenous Bmp2 partially rescued the delays in chondrocyte differentiation. Thus, H3.3K36M mutant proteins dominantly reprogram H3K36me2/me3 and chondrocyte gene expression, inhibiting terminal chondrocyte differentiation and contributing to tumorigenesis.

2016-10-06 | GSE75234 | 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