Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Deregulated expression programs in the hypomorphic Dnmt3b mutant mice

ABSTRACT: The function of Dnmt3b, of which deregulated activity is linked to several human pathologies, was studied using Dnmt3b hypomorphic mutant mice with reduced catalytic activity. Microarray analysis of deregulated expression programs in the hypomorphic Dnmt3b mutant mice (m3/m24) was combined to an analysis of the molecular mechanisms involved in the illegitimate activation of a specific set of genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE19597 | GEO | 2010/04/21

SECONDARY ACCESSION(S): PRJNA122383

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Deregulated expression programs in the hypomorphic Dnmt3b mutant mice

Project description:The function of Dnmt3b, of which deregulated activity is linked to several human pathologies, was studied using Dnmt3b hypomorphic mutant mice with reduced catalytic activity. Microarray analysis of deregulated expression programs in the hypomorphic Dnmt3b mutant mice (m3/m24) was combined to an analysis of the molecular mechanisms involved in the illegitimate activation of a specific set of genes. Mouse embryonic fibroblasts and thymus tissues isolated from 12.5 dpc and 18.5 dpc, respectively, wild-type and hypomorphic embryos (129SvJae x C57BL/6 hybrid genetic background). Total RNA was isolated using RNeasy Mini kit (QIAGEN), amplified, labeled, and hybridized following a previously described protocol (Le Brigand et al., Nuc Acid Res, 2006). Total RNA was coupled with Cyanine 3 or 5 and then hybridized in competition with reference RNA composed of a pool of total RNA isolated from wild-type thymus or MEF cells (thymus, n=5; MEF, n=5); two dye-swap were realized leading to the analysis of 18 microarrays for thymus (2 microarrays were excluded for unsufficient quality) and 20 for MEF cells. Arrays were then scanned with Agilent G2565AA Microarray Scanner (Agilent Technologies).

2010-04-21 | E-GEOD-19597 | biostudies-arrayexpress

Mus musculus

Project description:Deregulated expression programs in the hypomorphic Dnmt3b mutant mice

| PRJNA122383 | ENA

Bcl11b hypomorphic mutant thymocytes

Project description:Bcl11b hypomorphic mutant thymocytes

| PRJNA356604 | ENA

DNA methyltransferase 3B (DNMT3B) mutations in ICF syndrome: gene expression analysis

Project description:Genome-wide DNA methylation patterns are established and maintained by the coordinated action of three DNA methyltransferases, DNMT1, DNMT3A, and DNMT3B. DNMT3B hypomorphic germline mutations are responsible for two-thirds of Immunodeficiency, Centromere Instability, Facial Anomalies (ICF) syndrome cases. The molecular defects in transcription, DNA methylation, and chromatin structure in ICF cells remain relatively uncharacterized. We used expressing microarrays to define the global program of gene expression to elucidate the role of DNMT3B in these processes using EBV-immortalized lymphoblastoid cell lines (LCLs) derived from ICF syndrome and normal individuals. Keywords: disease-state analysis

2007-11-01 | GSE9499 | GEO

expression comparison of wildtype lungs and hypomorphic for nmyc

Project description:comparison of expression of wildtype lungs and lungs with hypomorphic expression of nmyc. the lungs were pooled from several biological samples. The hypomorphoic mutant was orignally published in Moens CB et al [PMID: 1577267]. this is part of a larger collection of data comparing nmyc misexpression in the lung (gain of fucntion) and protein expression in the hypomorphic lungs. Keywords: expression comparison

2007-04-24 | GSE6079 | GEO

Genomic profiling of DNA methyltransferases reveals a role for DNMT3B in genic methylation

Project description:DNA methylation is an epigenetic modification associated with transcriptional repression of promoters and is essential for mammalian development. Establishment of DNA methylation is mediated by the de novo DNA methyltransferases DNMT3A and DNMT3B, whereas DNMT1 ensures maintenance of methylation through replication. Absence of these enzymes is lethal, and somatic mutations in these genes have been associated with several human diseases. How genomic DNA methylation patterns are regulated remains poorly understood, as the mechanisms that guide recruitment and activity of DNMTs in vivo are largely unknown. To gain insights into this matter we determined chromosomal binding and site-specific activity of the mammalian de novo DNA methyltransferases DNMT3A and DNMT3B. We show that both enzymes localize to methylated, CpG dense regions in mouse stem cells, yet are excluded from active promoters and enhancers. By specifically measuring sites of de novo methylation, we observe that enzymatic activity reflects chromosomal binding. De novo methylation increases with CpG density, yet is excluded from nucleosomes. Notably, we observed selective binding of DNMT3B to the bodies of transcribed genes, which leads to their preferential methylation. This targeting to transcribed sequences requires SETD2-mediated methylation of lysine 36 on histone H3 and a functional PWWP domain of DNMT3B. Together these findings reveal how sequence and chromatin cues guide de novo methyltransferase activity to ensure methylome integrity. Genome-wide binding analysis for biotin-tagged DNMT3A2 and DNMT3B and variants in wild type ES, wild type neuroprogenitor cells, ES cells triple-KO for Dnmt1,3a,3b and ES cell mutant for Setd2

2015-01-20 | E-GEOD-57412 | biostudies-arrayexpress

Methylation and gene expression data obtained from Dnmt3b+/- peripheral T-cell lymphomas.

Project description:Dnmt3b is a tumor suppressor in oncogene-driven lymphoid and myeloid malignancies in mice. However, it is poorly understood whether reduced Dnmt3b activities can initiate malignant hematopoiesis. We modulated Dnmt3b activity in vivo by generating Dnmt3b+/− mice expressing one wild-type allele. Here, we analyzed methylation and gene expression in Dnmt3b+/- peripheral T-cell lymphomas (PTCLs).

2020-12-31 | GSE154270 | GEO

Transcription profiling of mouse wildtype lungs vs. lung hypomorphic for nmyc

2008-06-14 | E-GEOD-6079 | biostudies-arrayexpress

DNMT3B PWWP mutations cause hypermethylation of heterochromatin (T7-DNMT3B ChIP-seq)

Project description:The correct establishment of DNA methylation patterns is vital for mammalian development and is achieved by the de novo DNA methyltransferases DNMT3A and DNMT3B. DNMT3B localises to H3K36me3 at actively transcribing gene bodies through its PWWP domain. It also functions at heterochromatin through an unknown recruitment mechanism. Here we find that knockout of DNMT3B causes losses of methylation predominantly at H3K9me3-marked heterochromatin and that DNMT3B PWWP domain mutations or deletion result in striking increases of methylation in H3K9me3-marked heterochromatin. Removal of the N-terminal region of DNMT3B affects its ability to methylate H3K9me3-marked regions. This region of DNMT3B directly interacts with HP1-alpha and facilitates the bridging of DNMT3B with H3K9me3-marked nucleosomes in vitro. Our results suggest that DNMT3B is recruited to H3K9me3 marked heterochromatin in a PWWP-independent manner that is facilitated by the protein's N-terminus through an interaction with a key heterochromatin protein. More generally, we suggest that DNMT3B plays a role in DNA methylation homeostasis at heterochromatin, a process which is disrupted in cancer, aging and Immunodeficiency, Centromeric Instability and Facial Anomalies (ICF) syndrome.

2024-01-22 | GSE244516 | GEO

DNA methylation analysis and expression profiling during murine embryogenesis and in embryos deficient for DNMT3A or DNMT3B

Project description:We quantified the targets and kinetics of DNA methylation acquisition in mouse embryos, and determined the contribution of the de novo methyltransferases DNMT3A and DNMT3B to this process. We provide single-base maps of cytosine methylation by RRBS from the blastocysts to post-implantation stages and in embryos lacking DNMT3A or DNMT3B activity, and performed RNA-Seq in embryos lacking DNMT3B activity. We sequenced RRBS libraries prepared from genomic DNA isolated from embryos at consecutive stages of development between E3.5 and E11.5,and adult differentiated cells (sperm, liver). We performed RRBS on blastocysts at E3.5/E4.5, dissected epiblasts at E5.5/E6.5/E7/5, whole embryos at E8.5/E10.5 and limbs at E11.5. RRBS experiments in Dnmt3a-/- and Dnmt3b-/- embryos were performed in biological duplicates on individual embryos. We sequenced RNA-Seq libraries prepared from total RNAs of three WT and Dnmt3b-/- littermate embryos collected at E8.5.

2014-11-14 | E-GEOD-60334 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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