This SuperSeries is composed of the SubSeries listed below.
Research resource: progesterone receptor targetome underlying mammary gland branching morphogenesis.
Sex, Age, Specimen part, Treatment
View SamplesProgesterone (P) acting through its cognate nuclear receptors (PRs) plays an essential role in driving pregnancy-associated branching morphogenesis of the mammary gland. However, the fundamental mechanisms, including global cistromic and acute genomic transcriptional responses that are required to elicit active branching morphogenesis in response to P, have not been elucidated. We used microarray analysis to identify global gene expression signatures that are acutely regulated by PRs in the mouse mammary gland after acute P treatment.
Research resource: progesterone receptor targetome underlying mammary gland branching morphogenesis.
Sex, Age, Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome Wide Mapping of NR4A Binding Reveals Cooperativity with ETS Factors to Promote Epigenetic Activation of Distal Enhancers in Acute Myeloid Leukemia Cells.
Cell line, Treatment
View SamplesNR4As are critical tumor suppressors of acute myeloid leukemia (AML) whose expression is broadly silenced in leukemia initiating cell enriched populations from human patients relative to normal hematopoietic stem/progenitor cells. Rescued NR4A expression in human AML cells inhibits proliferation and reprograms AML gene signatures via transcriptional mechanisms that remain to be elucidated. By intersecting an acutely regulated, NR4A1 dependent transcriptional profile with genome wide NR4A binding distribution, we now identify an NR4A targetome of 685 genes that are directly regulated by NR4A1. We show that NR4As regulate gene transcription primarily through interaction with distal enhancers that are co-enriched for both NR4A1 and ETS transcription factor motifs. Using a subset of NR4A activated genes, we demonstrate that the ETS factors ERG and FLI-1 are required for activation of NR4A bound enhancers and NR4A target gene induction. NR4A1 dependent recruitment of ERG and FLI-1 promotes binding of p300 histone acetyl transferase to activate NR4A bound enhancers. These findings disclose novel epigenetic mechanisms by which NR4As and ETS factors cooperate to drive NR4A dependent gene transcription in human AML cells.
Genome Wide Mapping of NR4A Binding Reveals Cooperativity with ETS Factors to Promote Epigenetic Activation of Distal Enhancers in Acute Myeloid Leukemia Cells.
Cell line, Treatment
View SamplesActin dynamically shuttles between the nucleus and cytosplasm and regulates a wide range of transcriptional processes within the nucleus
Nuclear actin modulates cell motility via transcriptional regulation of adhesive and cytoskeletal genes.
Specimen part, Cell line
View SamplesWe investigated the effects of a single pulse of growth hormone on the transcriptional activation of STAT5 target genes in hypophysectomized male mouse liver. This GEO series is part of a larger study, where we investigated the impact of a single pulse of GH given to hypophysectomized mice on local liver chromatin accessibility [DNase hypersensitive site analysis], transcription rates [hnRNA analysis], and gene expression [quantitative PCR and RNA-Seq] determined 30, 90 or 240 min later. The STAT5-dependent but sex-independent early GH response genes Igf1 and Cish showed rapid, GH pulse-induced increases in chromatin accessibility and gene transcription, reversing the effects of hypophysectomy. Rapid increases in liver chromatin accessibility and transcriptional activity were also induced in hypophysectomized male mice for some (Ces2b, Ugt2b38) but not for other liver STAT5-dependent male-biased genes (Cyp7b1). Moreover, in pituitary-intact male mice, Igf1, Cish, Ces2b and Ugt2b38 all showed remarkable cycles of chromatin opening and closing, and associated cycles of induced gene transcription, which closely followed each endogenous pulse of liver STAT5 activity. Thus, the endogenous rhythms of male plasma GH pulsation dynamically open and then close liver chromatin at discrete, localized regulatory sites in temporal association with transcriptional activation of Igf1, Cish and a subset of STAT5-dependent male-biased genes. Overall design: Liver RNA was isolated from hypophysectomized male mice that were untreated, or were treated with a single pulse of GH and euthanized 30, 90 or 240 minutes later. 8 Individual RNA samples were pooled to make 2 biological replicates per condition for RNA-seq analysis.
Activation of Male Liver Chromatin Accessibility and STAT5-Dependent Gene Transcription by Plasma Growth Hormone Pulses.
Sex, Age, Specimen part, Cell line, Treatment, Subject
View SamplesWe investigated the effects of a single pulse of growth hormone on the transcriptional activation of STAT5 target genes in hypophysectomized male mouse liver. This GEO series is part of a larger study, where we investigated the impact of a single pulse of GH given to hypophysectomized mice on local liver chromatin accessibility [DNase hypersensitive site analysis], transcription rates [hnRNA analysis], and gene expression [quantitative PCR and RNA-Seq] determined 30, 90 or 240 min later. The STAT5-dependent but sex-independent early GH response genes Igf1 and Cish showed rapid, GH pulse-induced increases in chromatin accessibility and gene transcription, reversing the effects of hypophysectomy. Rapid increases in liver chromatin accessibility and transcriptional activity were also induced in hypophysectomized male mice for some (Ces2b, Ugt2b38) but not for other liver STAT5-dependent male-biased genes (Cyp7b1). Moreover, in pituitary-intact male mice, Igf1, Cish, Ces2b and Ugt2b38 all showed remarkable cycles of chromatin opening and closing, and associated cycles of induced gene transcription, which closely followed each endogenous pulse of liver STAT5 activity. Thus, the endogenous rhythms of male plasma GH pulsation dynamically open and then close liver chromatin at discrete, localized regulatory sites in temporal association with transcriptional activation of Igf1, Cish and a subset of STAT5-dependent male-biased genes. Overall design: Liver RNA was isolated from untreated hypophysectomized male mice and from hypophysectomized male mice treated with a single pulse of GH and euthanized 30, 90 or 240 minutes later. 8 Individual RNA samples were pooled to make 2 biological replicates per condition for RNA-seq analysis.
Activation of Male Liver Chromatin Accessibility and STAT5-Dependent Gene Transcription by Plasma Growth Hormone Pulses.
Sex, Age, Specimen part, Cell line, Treatment, Subject
View SamplesRNAseq analysis of caecal tissue from 14 C. jejuni-susceptible and 14 C. jejuni-resistant birds from a single population of infected chickens was conducted in order to identify gene expression associated with resistance to colonization. Significantly higher expression of genes involved in the innate immune response, cytokine signaling, B cell and T cell activation and immunoglobulin production, as well as the renin-angiotensin system was observed in resistant birds. Overall design: A population of 255 Barred Rock chickens were orally inoculated with C. jejuni and their caecal colonization levels estimated 48 hours post-inoculation. Caecal samples from 14 birds with no colonization and the 14 birds with the highest colonization were selected for mRNA sequencing.
Genome-wide association analysis of avian resistance to Campylobacter jejuni colonization identifies risk locus spanning the CDH13 gene.
Specimen part, Subject
View SamplesTranscriptomic changes in human liver cancer cell lines caused by the demethylating drug zebularine.
An integrated genomic and epigenomic approach predicts therapeutic response to zebularine in human liver cancer.
Cell line
View SamplesCells can survive effector caspase (caspase 3/7) activation in response to transient apoptotic stimuli, a process named anastasis. To characterize the molecular events that occur during anastasis, we performed whole transcriptome RNA sequencing of untreated, apoptotic, and recovering cells. We found that anastasis is an active, two-stage program with unique transcriptional profiles in each stage. We also identified 10 genes that specific to the early stage of anastasis. Overall design: 3hr ethanol treatment was used to induce apoptosis in Hela cells. Ethanol was washed away after 3hr treatment to allow cells to recover. Total RNA was prepared from mock-treated cells, ethanol-treated cells and cells after 1hr, 2hr, 3hr, 4hr, 8hr, 12hr recovery, followed by ribosomal RNA depletion. 3 biological replicates were included for each group. Sequencing was done using Ion Proton.
A molecular signature for anastasis, recovery from the brink of apoptotic cell death.
Cell line, Treatment, Subject
View Samples