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DNA hypomethylation leads to derepression of myeloerythroid genes in hematopoietic stem cells (HSC)

ABSTRACT: Analysis of hematopoietic stem cells (HSC, LSK Flt3-) and myeloid progenitors (MP, LK CD34+) sorted from wildtype and Dnmt1 hypomorph mice

ORGANISM(S): Mus musculus

PROVIDER: GSE17765 | GEO | 2009/10/06

SECONDARY ACCESSION(S): PRJNA118313

REPOSITORIES: GEO

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Transcription profiling of mouse hematopoietic stems cells and myeloid progenitor cells from wild type and Dnmt1 hypomorph mice shows DNA hypomethylation leads to derepression of myeloerythroid genes

Project description:Analysis of hematopoietic stem cells (HSC, LSK Flt3-) and myeloid progenitors (MP, LK CD34+) sorted from wildtype and Dnmt1 hypomorph mice Experiment Overall Design: We FACS sorted HSCs and MPs from bone marrow of 8-12 week old wildtype or Dnmt1 hypomorph (Dnmt1-/chip) mice.

2009-10-09 | E-GEOD-17765 | biostudies-arrayexpress

Deep proteomic analysis of Dnmt1 mutant/hypomorphic colorectal cancer cells reveals dys-regulation of Epithelial-Mesenchymal Transition and subcellular re-localization of Beta-Catenin

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Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis

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Transcription profiling of mouse bone marrow hematopoietic stem cell CD34 Flt3 subfractions

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Expression data from WT and E2A-KO bone marrow stem and progenitor cell subfractions.

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Transcription profiling of mouse WT and E2A-KO bone marrow stem and progenitor cell subfractions.

Project description:Expression profiling of WT and E2A-KO LSK FLT3- and LMPP protenitor cells. Experiment Overall Design: LSK FLT3- and LMPP stem/progenitor cells from WT and E2A-KO mice were FACS sorted. Subsequently RNA was extracted, labelled and hybridized to Affymetrix microarrays. Goal of experiment was to investigate expression changes between WT and KO LMPP cells.

2008-10-25 | E-GEOD-11982 | biostudies-arrayexpress

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A mutant DNMT1 enhances tumorigenicity with focal hypermethylation and global hypomethylation

Project description:Site-specific hypermethylation of tumor suppressor genes accompanied by genome-wide hypomethylation are epigenetic hallmarks of malignancy. However, molecular mechanisms that drive these linked changes in DNA methylation remain obscure. DNA methyltransferase 1 (DNMT1), the principle enzyme responsible for maintaining methylation patterns is commonly dysregulated in tumors. Replication foci targeting sequence (RFTS) is an N-terminal domain of DNMT1 that inhibits DNA-binding and catalytic activity, suggesting that RFTS deletion would result in gain of DNMT1 function. However, earlier data suggested that RFTS is required for DNMT1 activity. Here, we determined cellular consequences of RFTS deletion from DNMT1 in immortalized human bronchial epithelial cells. Compared to full-length DNMT1, ectopic expression of DNMT1- ?RFTS caused greater malignant transformation and enhanced promoter methylation that silenced DAPK and DUOX1 gene expression and increased intensity of promoter methylation across the genome. Strikingly, DNMT1-?RFTS also produced genomic hypomethylation and demethylation of Satellite 2 repeat sequences. Because deletion of RFTS is sufficient to induce focal hypermethylation and global hypomethylation in parallel, evidence suggests that the RFTS domain is a target responsible for epigenetic changes in cancer. DNA samples from HBEC3 cells transfected with vector control and HBEC3 cells with full-length and RFTS-deleted DNMT1 were assessed for genome-wide methylation using the microarray-based high resolution HpaII tiny fragment enriched by ligation-mediated PCR (HELP) assay.

2014-09-30 | E-GEOD-57829 | biostudies-arrayexpress

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Project description:Site-specific hypermethylation of tumor suppressor genes accompanied by genome-wide hypomethylation are epigenetic hallmarks of malignancy. However, molecular mechanisms that drive these linked changes in DNA methylation remain obscure. DNA methyltransferase 1 (DNMT1), the principle enzyme responsible for maintaining methylation patterns is commonly dysregulated in tumors. Replication foci targeting sequence (RFTS) is an N-terminal domain of DNMT1 that inhibits DNA-binding and catalytic activity, suggesting that RFTS deletion would result in gain of DNMT1 function. However, earlier data suggested that RFTS is required for DNMT1 activity. Here, we determined cellular consequences of RFTS deletion from DNMT1 in immortalized human bronchial epithelial cells. Compared to full-length DNMT1, ectopic expression of DNMT1- ΔRFTS caused greater malignant transformation and enhanced promoter methylation that silenced DAPK and DUOX1 gene expression and increased intensity of promoter methylation across the genome. Strikingly, DNMT1-ΔRFTS also produced genomic hypomethylation and demethylation of Satellite 2 repeat sequences. Because deletion of RFTS is sufficient to induce focal hypermethylation and global hypomethylation in parallel, evidence suggests that the RFTS domain is a target responsible for epigenetic changes in cancer.

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