C. elegans totalRNA profiles of worms treated with RNAi for different Integrator complex genes or L4440 (Control). Worms were grown at 15ºC and samples were taken six days after silencing Overall design: C. elegans totalRNA profiles of worms treated with RNAi for different Integrator complex genes or L4440 (Control). Three replicates per sample. Deep sequencing in Illumina HiSeq1500.
Disruption of the Caenorhabditis elegans Integrator complex triggers a non-conventional transcriptional mechanism beyond snRNA genes.
Subject
View SamplesThe transcriptomes of model organisms have been defined under specific laboratory growth conditions. The standard protocol for Caenorhabditis elegans growth and maintenance is 20ºC on an Escherichia coli diet. Temperatures ranging from 15ºC to 25ºC or feeding with other species of bacteria are considered physiological lab conditions, but the effect of these conditions on the worm transcriptome have not been well characterized. Here, we compare the global patterns of gene expression for the reference Caenorhabditis elegans strain (N2) grown at 15oC, 20oC, and 25oC on two different diets, Escherichia coli and Bacillus subtilis. When C. elegans were fed E. coli and the growth temperature was increased, we observed an enhancement of defense response pathways and down-regulation of genes associated with metabolic functions. However, when C. elegans were fed B. subtilis and the growth temperature was increased, the nematodes exhibited a decrease in defense response pathways and an enhancement of expression of genes associated with metabolic functions. Our results show that C. elegans undergo significant metabolic and defense response changes when the maintenance temperature fluctuates within the physiologically accepted experimental range and that the degree of pathogenicity of the bacterial diet can further alter the worm transcriptome. Overall design: C. elegans mRNA profiles at different temperatures and feeding in six samples, three replicates per sample. Deep sequencing in Illumina HiSeq2500.
Effect of the diet type and temperature on the <i>C. elegans</i> transcriptome.
Subject
View SamplesAfter inactivation of Hoxa5 at postnatal days (P)1-P4, we established RNA-seq profiling with RNA extracted from P21 brainstem of tamoxifen-treated Hoxa5flox/flox;CMV-CreERT2+/- (Hoxa5 cKO) pups and tamoxifen-treated Hoxa5flox/flox;CMV-CreERT2-/-(Hoxa5 control) pups Overall design: To explore HOXA5 downstream target genes in the postnatal brainstem, we carried out transcriptomic analyses by RNA-Seq using a model of postnatal Hoxa5 loss-of-function. We induced Hoxa5 inactivation after birth (P1 to P4) using the tamoxifen-inducible CMV-CreERT2 mice and conditional Hoxa5 floxed allele mice (Hoxa5flox). RNA was extracted from the brainstem of P21 tamoxifen-treated Hoxa5flox/flox;CMV-CreERT2+/- pups and from tamoxifen-treated Hoxa5flox/flox;CMV-CreERT2-/- littermates (see extract protocol).
Conditional Loss of <i>Hoxa5</i> Function Early after Birth Impacts on Expression of Genes with Synaptic Function.
Specimen part, Treatment, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
NRASG12V oncogene facilitates self-renewal in a murine model of acute myelogenous leukemia.
Specimen part
View SamplesMutant RAS oncoproteins activate signaling molecules that drive oncogenesis in multiple human tumors including acute myelogenous leukemia (AML). However, the specific function of these pathways in AML is unclear. To elucidate the downstream functions of activated NRAS in AML, we employed a murine model of AML harboring Mll-AF9 and NRASG12V. We found that NRASG12V enforced leukemia self-renewal gene expression signatures and was required to maintain an MLL-AF9 and MYB-dependent gene expression program. In a multiplexed analysis of RAS-dependent signaling intermediates, the leukemia stem cell compartment was preferentially sensitive to RAS withdrawal. Use of RAS-pathway inhibitors showed that NRASG12V maintained leukemia self-renewal through mTOR and MEK pathway activation, implicating these pathways as potential targets for cancer stem cell-specific therapies. Overall design: Primary leukemia cells harvested from spleens were sorted into immunophenotypic subpopulations (Mac-1High, Mac-1LowKit–Sca-1–, Mac-1LowKit+Sca-1–, and Mac-1LowKit+Sca-1+). RNA was extracted from this subpopulations of cells and submitted for RNA sequencing.
NRASG12V oncogene facilitates self-renewal in a murine model of acute myelogenous leukemia.
No sample metadata fields
View SamplesMutant RAS oncoproteins activate signaling molecules that drive oncogenesis in multiple human tumors including acute myelogenous leukemia (AML). However, the specific function of these pathways in AML is unclear. To elucidate the downstream functions of activated NRAS in AML, we employed a murine model of AML harboring Mll-AF9 and NRASG12V. We found that NRASG12V enforced leukemia self-renewal gene expression signatures and was required to maintain an MLL-AF9 and MYB-dependent gene expression program. In a multiplexed analysis of RAS-dependent signaling intermediates, the leukemia stem cell compartment was preferentially sensitive to RAS withdrawal. Use of RAS-pathway inhibitors showed that NRASG12V maintained leukemia self-renewal through mTOR and MEK pathway activation, implicating these pathways as potential targets for cancer stem cell-specific therapies.
NRASG12V oncogene facilitates self-renewal in a murine model of acute myelogenous leukemia.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Cell-type-specific control of enhancer activity by H3K9 trimethylation.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Role of cell-type specific nucleosome positioning in inducible activation of mammalian promoters.
Specimen part, Treatment
View SamplesThe goal of this study is to compare the transcriptome of the 2 MVT1 subpopulations in order to identify new genes and pathways that stands beyond the CD24+ aggressive phenotype Overall design: mRNA profiles of CD24- and CD24+ cells were generated by deep sequencing, in triplicate, using Illumina HiSeq 2500
Deep sequencing of mRNA in CD24(-) and CD24(+) mammary carcinoma Mvt1 cell line.
No sample metadata fields
View SamplesIn dendritic cells, expression of the H3K9me3 demethylase JmjD2d is upregulated by LPS stimulation. To identify genes whose induction by LPS depends on JmjD2d activity, we performed a microarray analysis of wild-type and JmjD2d-knockdown dendritic cells, before and after stimulation with LPS.
Cell-type-specific control of enhancer activity by H3K9 trimethylation.
No sample metadata fields
View Samples