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Expression data from murine fibroblasts overexpressing Fbxl10

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE34691 | GEO | 2012/10/05

SECONDARY ACCESSION(S): PRJNA150295

REPOSITORIES: GEO

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Expression data from murine fibroblasts overexpressing Fbxl10

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.

2012-10-05 | E-GEOD-34691 | biostudies-arrayexpress

Fbxl10 regulates PRC1 recruitment to CpG islands and H2A ubiquitination

Project description:Polycomb repressive complex 1 (PRC1) catalyzes H2A monoubiquitination (uH2A) and regulates pluripotency in embryonic stem cells (ESCs). However the mechanisms controlling PRC1 recruitment and activity are largely unknown. Here we show that Fbxl10 interacts with Ring1B and Nspc1, forming a non-canonical PRC1. We demonstrate that Fbxl10-PRC1 is essential for H2A ubiquitination in mouse ESCs. Genome-wide analyses reveal that Fbxl10 preferentially binds to CpG islands and co-localizes with Ring1B on Polycomb target genes. Notably, Fbxl10 depletion causes modest dissociation of Ring1B but a major loss of uH2A on target genes. Furthermore rescue experiments for Fbxl10 reveal that its DNA binding capability and integration into PRC1 are required for proper H2A ubiquitination. ES cells lacking Fbxl10, like previously characterized Polycomb mutants, show a severely compromised capacity for successful differentiation. Our results shed light on a novel mechanism how CpG islands regulate chromatin function by affecting polycomb recruitment and activity. All ChIP-seq reactions were performed in either untransfected cells, cells expressing scrambled shRNA or Fbxl10 shRNA, Ring1b-/- or Suz12-/- mouse ES cells

2012-12-31 | E-GEOD-37930 | biostudies-arrayexpress

Overexpression of histone demethylase Fbxl10 leads to enhanced migration in mouse embryonic fibroblasts

Project description:Cell migration is a central process in the development and maintenance of multicellular organisms. Tissue formation during embryonic development, wound healing, immune responses and invasive tumors all require the orchestrated movement of cells to specific locations. Histone demethylase proteins alter transcription by regulating the chromatin state at specific gene loci. FBXL10 is a conserved and ubiquitously expressed member of the JmjC domain-containing histone demethylase family and is implicated in the demethylation of H3K4me3 and H3K36me2 and thereby removing active chromatin marks. However, the physiological role of FBXL10 in vivo remains largely unknown. Therefore, we established an inducible gain of function model to analyze the role of Fbxl10 and compared wild-type with Fbxl10 overexpressing mouse embryonic fibroblasts (MEFs). Our study shows that overexpression of Fbxl10 in MEFs doesn`t influence the proliferation capability but leads to an enhanced migration capacity in comparison to wild-type MEFs. Transcriptome and ChIP-seq experiments demonstrated that Fbxl10 binds to genes involved in migration like Areg, Mdk, Lmnb1, Thbs1, Mgp and Cxcl12. Taken together, our results strongly suggest that Fbxl10 plays a critical role in migration by binding to the promoter region of migration-associated genes and thereby might influences cell behaviour to a possibly more aggressive phenotype.

2016-10-01 | GSE86090 | GEO

FBXL10 and the Protection of Polycomb-bound Genes from Hypermethylation (RRBS)

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.

2015-04-06 | GSE65580 | GEO

Fbxl10 regulates PRC1 recruitment to CpG islands and H2A ubiquitination

2012-12-31 | GSE37930 | GEO

FBXL10 and the Protection of Polycomb-bound Genes from Hypermethylation (RNA-Seq)

2015-04-06 | GSE65582 | GEO

ChIP-Seq-Data from MEFs overexpressing Fbxl10

Project description:Overexpression of Fbxl10 leads to enhanced migration in mouse embryonic fibroblast

2016-10-01 | GSE76209 | GEO

Abnormal X chromosome inactivation and sex-specific gene dysregulation after ablation of FBXL10

Project description:The FBXL10 protein (also known as KDM2B, JHDM1B, CXXC2, and NDY1) is bound to essentially all CpG-rich promoters in the mammalian genome. FBXL10 is expressed as two isoforms: FBXL10-1, a longer form that contains an N-terminal JmjC domain with C- terminal F-box, CXXC, PHD, RING, and leucine rich repeat (LRR) domains, and FBXL10-2, a shorter form that initiates at an alternative internal exon and which lacks the JmjC domain but retains the other domains. Selective deletion of Fbxl10-1 had been reported to produce a minor and variable phenotype, and most mutant animals were essentially normal. We show here that deletion of Fbxl10-2 (in a manner that does not perturb expression of Fbxl10-1) resulted in a very different phenotype with craniofacial abnormalities, greatly increased lethality, and female sterility in surviving homozygous mutants. The phenotype of the Fbxl10-2 deletion was more severe in female mutants. We found that mutants that lacked both FBXL10-1 and -2 showed embryonic lethality and even more extreme sexual dimorphism, with more severe gene dysregulation in mutant female embryos. X-linked genes were most severely dysregulated, and there was marked overexpression of Xist in mutant females although genes that encode factors that bind to Xist RNA were globally down-regulated in mutant female as compared to male embryos. FBXL10 is the first factor shown to be required both for the normal expression and function of the Xist gene.

2016-05-31 | GSE76552 | GEO

Expression data from Fbxl10 overexpressing 3T3-L1 cells

Project description:Target genes of Fbxl10 during 3T3-L1 adipogenesis was analyzed

2015-03-04 | GSE64154 | GEO

Expression data from Fbxl10 overexpressing 3T3-L1 cells

Project description:Target genes of Fbxl10 during 3T3-L1 adipogenesis was analyzed 3T3-L1 cells overexpressing Fbxl10 using retrovirus system containing LTR promoter were differentiated and RNA was extracted at day 2 of differentiation

2015-03-04 | E-GEOD-64154 | biostudies-arrayexpress

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