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Retinoids induce rapid dynamic changes in the non-coding RNAs and epigenetic profiles of murine Hox clusters (tiling)

ABSTRACT: Physiologically relevant concentrations of retinoic acid are added to Mouse ES cells and a time course (0-72 hours) is examined with expression tiling arrays to characterize the early dynamics of expression of coding and non-coding RNAs in and around the Hox clusters. Gene expression is examined at various timepoints (0-72 hrs) after retinoic acid induced neuronal differentiation

ORGANISM(S): Mus musculus

SUBMITTER: Madelaine Gogol

PROVIDER: E-GEOD-61585 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Retinoids induce rapid dynamic changes in the non-coding RNAs and epigenetic profiles of murine Hox clusters.

Project description:Physiologically relevant concentrations of retinoic acid are added to Mouse ES cells and a time course (0-72 hours) is examined with expression tiling arrays and RNA-seq to characterize the early dynamics of expression of coding and non-coding RNAs in and around the Hox clusters. Gene expression is examined at various timepoints (0-72 hrs) after retinoic acid induced neuronal differentiation

2015-04-27 | E-GEOD-67610 | biostudies-arrayexpress

Retinoic acid (RA) induction time-course to profile gene expression during mES cell differentiation.

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Characterization of the coding and noncoding transcriptome in undifferentiated and differentiating mouse embryonic stem cells

Project description:RNA (poly(A)+ fraction) has ben isolated from undifferentiated mouse embryonic stem cells and from embryonic stem cells induced to differentiate using the hanging drop model, 6 days following iinduction of differentiation. Profiling of the transcritome at these two stages of differentiation using deep RNA sequencing allows identifying modulated coding and noncoding transcripts upon induction of differentiation. RNA profiling of mouse embryonic stem cells at two stages of differentiation, i.e. undifferntiated state and at day 6 after induction of differentiation. Two conditions, three biological replicates per condition

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Mammalian Dpy-30 regulates genomic H3K4 methylation and is essential for ES cell fate specification

Project description:H3K4 methylation is associated with active genes and, along with H3K27 methylation, is part of a bivalent chromatin mark that typifies poised developmental genes in ESCs. However, its functional roles in ESC maintenance and differentiation are not established. Here we show that mammalian Dpy-30, a core subunit of SET1/MLL complexes, biochemically modulates H3K4 methylation in vitro, and directly regulates chromosomal H3K4me3 throughout the mammalian genome. Depletion of Dpy-30 does not affect ESC self-renewal, but significantly alters the differentiation potential of ESCs, particularly along the neural lineage. The differentiation defect is accompanied by defects in gene induction and H3K4 methylation at key developmental loci. Our results provide strong experimental evidence for the hypothesis that H3K4 methylation is an essential functional component of the bivalent mark during activation of developmental genes in ESCs. Total RNAs from control or knockdown cells before and after RA-mediated differentiation were subjected to Illumina microarray analyses. ChIP-enriched DNA from mouse ES cells was analyzed by Solexa sequencing.

2011-02-01 | E-GEOD-26136 | biostudies-arrayexpress

AMPK governs lineage specification through Tfeb-dependent regulation of lysosomes

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2016-03-09 | E-GEOD-77705 | biostudies-arrayexpress

KMT1E Mediated H3K9 Methylation Is Required for the Maintenance of Embryonic Stem Cells by Repressing Trophectoderm Differentiation

Project description:Dynamic regulation of histone methylation by methyltransferases and demethylases plays a central role in regulating the fate of embryonic stem (ES) cells. The histone H3K9 methyltransferase KMT1E, formerly known as ESET or Setdb1, is essential to embryonic development as the ablation of the Setdb1 gene results in peri-implantation lethality and prevents the propagation of ES cells. However, Setdb1- null blastocysts do not display global changes in H3K9 methylation or DNA methylation, arguing against a genome- wide defect. Here we show that conditional deletion of the Setdb1 gene in ES cells results in the upregulation of lineage differentiation markers, especially trophectoderm-specific factors, similar to effects observed upon loss of Oct3/4 expression in ES cells. We demonstrate that KMT1E deficiency in ES cells leads to a decrease in histone H3K9 methylation at and derepression of trophoblast-associated genes such as Cdx2. Furthermore, we find genes that are derepressed upon Setdb1 deletion to overlap with known targets of polycomb mediated repression, suggesting that KMT1E mediated H3K9 methylation acts in concert with polycomb controlled H3K27 methylation. Our studies thus demonstrate an essential role for KMT1E in the control of developmentally regulated gene expression programs in ES cells. Analysis of KMT1E-deficiency in mouse embryonic stem cells using a Setdb1 conditional allele and tamoxifen-inducible Cre/loxP recombination

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