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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

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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

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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

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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

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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.

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