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Enrichment profiles of Ser-5 phosphorylated RNA polymerase II (PolII S5p) in mouse female ES cells

ABSTRACT: 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 ‘Ohno’s hypothesis’). It is unknown whether any epigenetic mark or protein is involved in X upregulation in mammals. Ser-5 phosphorylated RNA polymerase II (PolII S5p) is required for transcription initiation. Chromatin immunoprecipitation combined with DNA tiling array analysis (ChIP-chip) of PolII S5p in mouse female ES cells with two active X chromosomes demonstrated a greater enrichment of RNA polymerase II on X-linked genes relative to autosomal genes, suggesting that enhanced transcription initiation may play a role in X upregulation.

ORGANISM(S): Mus musculus

PROVIDER: GSE30689 | GEO | 2011/07/19

SECONDARY ACCESSION(S): PRJNA154693

REPOSITORIES: GEO

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Enrichment profiles of Ser-5 phosphorylated RNA polymerase II (PolII S5p) in mouse female ES cells

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 ‘Ohno’s hypothesis’). It is unknown whether any epigenetic mark or protein is involved in X upregulation in mammals. Ser-5 phosphorylated RNA polymerase II (PolII S5p) is required for transcription initiation. Chromatin immunoprecipitation combined with DNA tiling array analysis (ChIP-chip) of PolII S5p in mouse female ES cells with two active X chromosomes demonstrated a greater enrichment of RNA polymerase II on X-linked genes relative to autosomal genes, suggesting that enhanced transcription initiation may play a role in X upregulation. Comparison of RNA PolII S5p enrichment on the X versus autosomes in mouse

2011-07-18 | E-GEOD-30689 | biostudies-arrayexpress

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 ‘Ohno’s hypothesis’). 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.

2013-03-05 | GSE44835 | GEO

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

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

2011-07-19 | GSE30690 | GEO

RNA stability controlled by m6A methylation provides X to autosome compensation in mammals [miCLIP2]

Project description:In therian mammals, X-chromosomal genes are expressed only from a single active X chromosome, both in males (XY) as well as females (XX). To compensate for this reduction in dosage compared to the evolutionary ancestral state on two autosomes, it has been proposed that genes from the active X chromosome exhibit dosage compensation (“Ohno’s hypothesis”). However, the existence and mechanism of X-to-autosome dosage compensation are still under debate. Here, we show that dosage compensation is achieved via differential N6-methyladenosine (m6A) RNA modification. X-chromosomal transcripts are reduced in m6A modifications and more stable compared to the autosomal counterparts. Acute depletion of m6A using a small molecule inhibitor differentially affects autosomal and X-chromosomal transcripts across sexes, cell types, tissues and species, resulting in perturbed dosage compensation. We propose that higher stability of X-chromosomal transcripts is directed by lower levels of m6A, indicating that mammalian dosage compensation occurs via epitranscriptomic RNA regulation.

2023-02-14 | GSE203652 | GEO

RNA stability controlled by m6A methylation provides X to autosome compensation in mammals [SLAM-seq]

2023-02-14 | GSE203648 | GEO

RNA stability controlled by m6A methylation provides X to autosome compensation in mammals [RNA-seq]

2023-02-14 | GSE203642 | GEO

RNA stability controlled by m6A methylation provides X to autosome compensation in mammals [DNA-seq]

2023-02-14 | GSE203637 | GEO

Allele-specific maps of RNA polymerase II phosphorylated at serine 5 in mouse cultured hybrid cells and mouse hybrid brain

Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of RNA polymerase II phosphorylated at serine 5 (PolII-S5p; the transcription initiation form) in female mouse cultured hybrid cells and female hybrid brain derived from mouse systems with skewed X inactivation based on crosses between C57BL/6J (BL6) and M. spretus. In these systems, alleles can be differentiated by frequent SNPs between mouse species, and the active X (Xa) compared to the haploid set of autosomes from the same species. To examine PolII-S5p occupancy in vivo, ChIP-seq was done in brain from an adult female F1 mouse in which the BL6 X is always active and the spretus X inactive. Uniquely mapped reads containing informative SNPs were assigned to each haploid chromosome set (BL6 or spretus) and were counted to establish allele-specific PolII-S5p occupancy profiles. We found that PolII-S5p allele-specific occupancy with or without normalization by input genomic DNA sequencing data showed that expressed genes on the Xa (>1RPKM) had 30% higher PolII-S5p peak levels at their promoters compared to autosomal genes from the same species (BL6). This result was confirmed by performing an independent allele-specific ChIP-seq analysis on fibroblasts derived from embryonic kidney (Patski cell line) that have the opposite X inactivation pattern from the brain sample, i.e. an Xa from M. spretus and an Xi from BL6. These findings suggest that transcription initiation of X-linked genes is enhanced to contribute to X upregulation in cell lines and in vivo. Examination of allele-specific PolII-S5p occupancy in mouse hybrid cells and brain.

2013-02-15 | E-GEOD-44255 | biostudies-arrayexpress

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