ChIP-Seq-Data from MEFs overexpressing Fbxl10
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE76209 | GEO | 2016/10/01
SECONDARY ACCESSION(S): PRJNA306643
REPOSITORIES: GEO
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Project description:Posttranslational modifications on histone tails control gene expresssion levels in an either positive or negative way. Therefore enzymes which modifiy the modifications on the histon tails, like histone demethylases, are able to strictly regulate the transcriptom. To analyse the regulatory role of histone demethylase Fbxl10 we generated a stable cell line permanently overexpressing HA-tagged Fbxl10 and identified the transcriptome changes compared to untransfected control cell line by microarray. Tet-off Mefs were transfected with a plasmid containing HA-Fbxl10 cDNA and a Hygromycin resistence plasmid and cell clones were selected for HA-Fbxl10 expression. Three independent RNA samples were generated from untransfected Tet-off Mef cells (C1-C3) and from Tet-off Mef HA-Fbxl10 (D1-D3) and hybridisated on Affymetrix microarray.
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Project description:Nearly all CpG-dense promoters are occupied by the multi-domain chromosomal protein FBXL10. We show here that complete inactivation of the Fbxl10 gene leads to dense de novo methylation only of the promoters that are co-occupied by both FBXL10 and by Polycomb Repressive Complexes; this results in pervasive defects in embryonic development and death of homozygous Fbxl10 mutant embryos at midgestation. Deletion of key components of Polycomb Repressive Complexes 1 and 2 did not lead to ectopic de novo methylation. These results indicate that FBXL10 defends Polycomb-occupied promoters against ectopic de novo methylation. FBXL10 is the first reported factor whose loss leads to a gain in genomic DNA methylation.
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Project description:Nearly all CpG-dense promoters are occupied by the multi-domain chromosomal protein FBXL10. We show here that complete inactivation of the Fbxl10 gene leads to dense de novo methylation only of the promoters that are co-occupied by both FBXL10 and by Polycomb Repressive Complexes; this results in pervasive defects in embryonic development and death of homozygous Fbxl10 mutant embryos at midgestation. Deletion of key components of Polycomb Repressive Complexes 1 and 2 did not lead to ectopic de novo methylation. These results indicate that FBXL10 defends Polycomb-occupied promoters against ectopic de novo methylation. FBXL10 is the first reported factor whose loss leads to a gain in genomic DNA methylation. DNA methylation analysis using RRBS and expression analysis using RNA-seq was performed on WT and Fbxl10T/T ES cells.
2015-04-06 | E-GEOD-65580 | biostudies-arrayexpress
Project description:Nearly all CpG-dense promoters are occupied by the multi-domain chromosomal protein FBXL10. We show here that complete inactivation of the Fbxl10 gene leads to dense de novo methylation only of the promoters that are co-occupied by both FBXL10 and by Polycomb Repressive Complexes; this results in pervasive defects in embryonic development and death of homozygous Fbxl10 mutant embryos at midgestation. Deletion of key components of Polycomb Repressive Complexes 1 and 2 did not lead to ectopic de novo methylation. These results indicate that FBXL10 defends Polycomb-occupied promoters against ectopic de novo methylation. FBXL10 is the first reported factor whose loss leads to a gain in genomic DNA methylation. DNA methylation analysis using RRBS and expression analysis using RNA-seq was performed on WT and Fbxl10T/T ES cells.
2015-04-06 | E-GEOD-65582 | biostudies-arrayexpress