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Expression data from mouse ES cells after control RNAi (scramble siRNAs) or RNAi specific for Kdm6a treatment.

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Joel Berletch

PROVIDER: E-GEOD-45034 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from mouse ES cells after control RNAi (scramble siRNAs) or specific RNAi (siRNAs for specific genes) treatment

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

Expression data from mouse ES cells after control RNAi (scramble siRNAs) or RNAi specific for Kdm6a treatment.

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

Protein and histone binding profiles from mouse ES cells during differentiation and after Kdm6a RNAi treatment.

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.

2013-03-22 | E-GEOD-45390 | biostudies-arrayexpress

Protein and histone binding profiles from mouse ES cells during differentiation and after Kdm6a RNAi treatment.

2013-03-22 | GSE45390 | GEO

Expression data from undifferentiated and differentiated mouse female ES cells PGK12.1

Project description:Affymetrix 430 2.0 mouse arrays were used for expression analyses in undifferentiated and differentiated PGK12.1 ES cells. We found that the X:autosome expression ratios calculated from the mean expression values of X-linked and autosomal genes from microarrays was ~1.4 in undifferentiated female ES cells and then decreased to 1.2 in PGK12.1 cells after 15-day embryoid body differentiation. Thus, a substantial level of X upregulation is already evident in these ES cells prior to differentiation. Our findings based on Affymetrix expression arrays are consistent with microarray analysis from other labs and our RNA-seq analysis of mouse female PGK12.1 ES cells. Mouse female ES cells PGK12.1 were differentiated by the EB (embryoid body) differentiation protocol. The presence of two active X chromosomes in undifferentiated female ES cells and one active X in 15-day differentiated cells was verified by Xist RNA FISH. Total RNA was prepared from undifferentiated and 15-day differentiated PGK12.1 and was used for expression array analyses to examine exprssion of the X chromosome during differentiation.

2013-02-15 | E-GEOD-44251 | biostudies-arrayexpress

Expression analysis in mouse female PGK12.1 ES cells by RNA-seq

Project description:Many animal species employ a chromosome-based mechanism of sex determination, which has led to coordinate evolution of dosage compensation systems. Dosage compensation not only corrects the imbalance in the number of X-chromosomes between the sexes, but is also hypothesized to correct dosage imbalance within cells due to mono-allelic X expression and bi-allelic autosomal expression, by upregulating X-linked genes (termed M-CM-"M-BM-^@M-BM-^XOhnoM-CM-"M-BM-^@M-BM-^Ys hypothesisM-CM-"M-BM-^@M-BM-^Y). Although this hypothesis is well supported by expression analyses of individual X-linked genes and by array-based transcriptome analyses, a recent study claimed that no such X upregulation exists in mammals and C. elegans based on RNA-sequencing and proteomics analyses. We provide RNA-seq RNA-seq analysis of mouse female PGK12.1 ES cells with two active X chromosomes and confirmed that the X chromosome is upregulated, consistent with the previous microarray study. Examination of expression of X-linked and autosomal genes in mouse female ES cells with two active X chromosomes.

2011-07-19 | E-GEOD-30690 | biostudies-arrayexpress

Expression regulation by RYBP in mouse embryonic stem cells

Project description:Polycomb repressive complexes (PRCs) are important chromatin regulators of ES cell function. RYBP binds Polycomb H2A monoubiquitin ligases Ring1A and Ring1B, and has been suggested to participate in localizing Polycomb complexes to their targets. Moreover, constitutive inactivation of RYBP precludes ES cell formation. Here we have used ES cells conditionally deficient in RYBP to investigate RYBP function. Chromosome immunoprecipitation on a chip (ChIP-chip) of RYBP and microarray experiments were performed using wild type and knocked-out ES cells. Gene expression profiling of WT, conditionally deficient in RYBP with or without Yaf2 RNAi, and ChIP-chip of RYBP on promoters of WT, Dnmt1-KO or Eed-KO ES cells.

2012-04-03 | E-GEOD-32294 | biostudies-arrayexpress

Gene expression analysis of HepG2 cells by NOTUM RNAi

Project description:We identified human NOTUM, a new member of beta-catenin target gene. The aim of this analysis is to examine downstream genes of NOTUM. Keywords: Gene expression analysis in response to RNA interference HepG2 cells with RNAi duplexed were used. One control (control-low GC) and 2 RNAi duplexes (NOTUM RNAi#1 and #2) for NOTUM silencing were added to HepG2 cells, and total RNAs were isolated at 72 hours after transfection.

2011-03-15 | E-GEOD-6368 | biostudies-arrayexpress

The production of Excretory-Secretory molecules from Heligmosomoides polygyrus bakeri fourth stage larvae varies between mixed and single sex cultures.

Project description:In this study, the composition of ES of male and female L4 stage Heligmosomoides polygyrus bakeri in the presence (cultured together) or absence (cultured alone) of the opposite sex was examined using mass spectrometry.

2021-09-10 | PXD023759 | Pride

Upregulation of the mammalian X chromosome is associated with enhanced transcription initiation, MOF-mediated H4K16 acetylation, and longer RNA half-life

Project description:Many animal species employ a chromosome-based mechanism of sex determination, which has led to coordinate evolution of dosage compensation systems. Dosage compensation not only corrects the imbalance in the number of X-chromosomes between the sexes, but is also hypothesized to correct dosage imbalance within cells due to mono-allelic X expression and bi-allelic autosomal expression, by upregulating X-linked genes (termed M-bM-^@M-^XOhnoM-bM-^@M-^Ys hypothesisM-bM-^@M-^Y). To identify molecular mechanisms of X upregulation in mammals we established genome-wide profiles for the initiation and elongation forms of RNA polymerase II (PolII), PolII-S5p (phosphorylated at serine 5) and PolII-S2p (phosphorylated at serine 2), and for histone modifications in mouse cell lines and tissues. We found that in addition to being enriched in PolII-S5p but not in PolII-S2p, X-linked promoters were also enriched in two epigenetic marks, H4K16ac and H2AZ, dependent on expression levels. To address the function of the H4K16 acetyltransferase MOF occupancy profiles were established and knockdowns of MOF and MSL1 were done in mouse ES cells. Our results support a conserved role for the MSL complex to enhance transcription initiation of X-linked genes. Comparison of the profiles of RNA PolII, the H4K16ac acetyltransferase MOF and histone active marks on the X versus autosomes in mouse

2013-03-05 | E-GEOD-44835 | biostudies-arrayexpress

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