Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA192883 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data from mouse ES cells after control RNAi (scramble siRNAs) or specific RNAi (siRNAs for specific genes) treatment
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Project description:To address the functional role of KDM6A in the regulation of Rhox genes, male and female mouse ES cells were transfected with a mixture of three small interfering RNA duplexes, each of which targets a different region of Kdm6a mRNA. We found that Kdm6a knockdown in mouse ES cells caused a decrease in expression of a subset of Rhox genes, Rhox6 and 9. Furthermore, Rhox6 and 9 expression was decreased in female ES cells but not male ES cells indicating that KDM6A regulates Rhox gene expression in a sexually dimorphic manner. Mouse ES cells were treated by Invitrogen scramble siRNA duplexes or specific siRNA duplexes and used for RNA extraction and hybridization on Affymetrix microarrays. Four RNA samples from two independent double-RNAi treatments and two single-RNAi treatment in undifferentiated female ES cells PGK12.1, and RNA samples from two single-RNAi treatments in undifferentiated male ES cells WD44 were assayed for expression changes by arrays.
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Project description:To address the functional role of MOF in mammalian X upregulation, male and female mouse ES cells were transfected with a mixture of three small interfering RNA duplexes, each of which targets a different region of Mof mRNA. We found that MOF knockdown in mouse ES cells caused a greater drop in expression of X-linked genes compared to autosomal genes, as measured by expression array analyses. The strongest effect was observed on medium-expressed X-linked genes. We next examined components of the two known MOF protein complexes, MSL1 (male-specific lethal1) and NSL1 (nonspecific lethal1). Knockdown of MSL1 but not NSL1 in undifferentiated female ES cells PGK12.1 specifically caused a decrease in expression levels of X-linked genes. Cells co-transfected with both MOF and MSL1 siRNAs had similar expression changes to MSL1 knockdown alone, indicating that these components probably operate within the same complex but are not additive. Our findings that key components of the MSL but not NSL complex play a role in upregulation of mammalian X-linked genes in ES cells. Mouse ES cells were treated by Invitrogen scramble siRNA duplexes or specific siRNA duplexes and used for RNA extraction and hybridization on Affymetrix microarrays. Six RNA samples from two independent double-RNAi treatments and one single-RNAi treatment in undifferentiated female ES cells PGK12.1, and RNA samples from two single-RNAi treatments in undifferentiated male ES cells WD44 or E14 were assayed for expression changes by arrays. RNA samples from three MSL1RNAi treatments, two MOF/MSL1RNAi treatments and three NSL1RNAi treatments in undifferentiated female ES cells PGK12.1 were assayed by arrays.
2013-02-15 | E-GEOD-44252 | biostudies-arrayexpress
Project description:Here we show binding and occupancy profiles for KDM6A, H3K27me3 and H3K4me3 to address the epigenetic regulation of a subset of Rhox genes, Rhox6 and 9, in female and male ES cells during differentiation. To further address a functional role for KDM6A in the epigenetic regulation of Rhox6 and 9, binding profiles for female ES cells treated with a control siRNA and siRNA specific for Kdm6a are shown. We report that two members of the Rhox cluster, Rhox6 and 9, are regulated by de-methylation of histone H3 at lysine 27 by KDM6A, a histone demethylase with female-biased expression. Our results are consistent with other homeobox genes in that Rhox6 and 9 are in bivalent domains prior to embryonic stem cell differentiation and thus poised for activation. In female mouse ES cells KDM6A is specifically recruited to Rhox6 and 9 for gene activation, a process inhibited by Kdm6a knockdown. In contrast, KDM6A occupancy at Rhox6 and 9 is low in male ES cells and knockdown has no effect on expression. Our study implicates Kdm6a, a gene that escapes X inactivation, in the regulation of genes important in reproduction, suggesting that KDM6A may play a role in the etiology of developmental and reproduction-related effects of X chromosome anomalies. ChIP-chip was used to analyze the binding profiles of KDM6A, H3K27me3, and H3K4me3 during differentiation in female and male ES cells. Additionally, ChiP-chip of KDM6A binding in control treated and siRNA treated ES cells is presented.
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Project description:Here we show binding and occupancy profiles for KDM6A, H3K27me3 and H3K4me3 to address the epigenetic regulation of a subset of Rhox genes, Rhox6 and 9, in female and male ES cells during differentiation. To further address a functional role for KDM6A in the epigenetic regulation of Rhox6 and 9, binding profiles for female ES cells treated with a control siRNA and siRNA specific for Kdm6a are shown. We report that two members of the Rhox cluster, Rhox6 and 9, are regulated by de-methylation of histone H3 at lysine 27 by KDM6A, a histone demethylase with female-biased expression. Our results are consistent with other homeobox genes in that Rhox6 and 9 are in bivalent domains prior to embryonic stem cell differentiation and thus poised for activation. In female mouse ES cells KDM6A is specifically recruited to Rhox6 and 9 for gene activation, a process inhibited by Kdm6a knockdown. In contrast, KDM6A occupancy at Rhox6 and 9 is low in male ES cells and knockdown has no effect on expression. Our study implicates Kdm6a, a gene that escapes X inactivation, in the regulation of genes important in reproduction, suggesting that KDM6A may play a role in the etiology of developmental and reproduction-related effects of X chromosome anomalies.
2013-03-22 | GSE45390 | GEO
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Project description:To address the functional role of KDM6A in the regulation of Rhox genes, male and female mouse ES cells were transfected with a mixture of three small interfering RNA duplexes, each of which targets a different region of Kdm6a mRNA. We found that Kdm6a knockdown in mouse ES cells caused a decrease in expression of a subset of Rhox genes, Rhox6 and 9. Furthermore, Rhox6 and 9 expression was decreased in female ES cells but not male ES cells indicating that KDM6A regulates Rhox gene expression in a sexually dimorphic manner.
2013-03-13 | GSE45034 | GEO