Gene expression data from control and REPTOR (=CG13624) KO male adults
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ABSTRACT:
ORGANISM(S): Drosophila melanogaster
SUBMITTER: Aurelio Teleman
PROVIDER: E-GEOD-64846 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The first aim was to identify genes whose transcription is induced by rapamycin feeding in Drosophila larvae. Secondly, the goal was to find out which contribution the transcription factor REPTOR (=CG13624) has to the observed changes in expression. We thus compared gene epxression between rapamycin fed and control fed larvae in wild type larvae and in REPTOR KO larvae. 3 biological replicates from 4 conditions: control larvae plus/miuns rapamycin, KO larvae plus/minus rapamycin; overall 12 samples
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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2015-04-30 | E-GEOD-55221 | biostudies-arrayexpress
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2015-11-05 | E-GEOD-74673 | biostudies-arrayexpress
Project description:The mechanism of egress of mature regulatory T cells (Tregs) from the thymus to the periphery remains enigmatic, as does the nature of those factors expressed in the thymic environment. Here, we examined the fate of thymic Tregs in TNFα/RelA double-knockout (TA-KO) mice, because TA-KO mice retain a Treg population in the thymus but have only a small Treg population at the periphery. Transplantation of whole TA-KO thymus to under the kidney capsule of Rag1 null mice failed to induce the production of donor-derived splenic Tregs expressing neuropilin-1 (Nrp1), which was reported to be a marker of naturally occurring Tregs, indicating that TA-KO thymic Tregs either do not leave the thymus or are lost at the periphery. We next transplanted enriched TA-KO thymic Tregs to the peripheries of TA-KO mice and traced mouse survival. Transplantation of TA-KO thymic Tregs rescued the lethality in TA-KO mice, demonstrating that TA-KO thymic Tregs remain functional at the periphery. The TA-KO thymic Treg population had highly demethylated CpG motifs in the foxp3 locus, indicating that the cells were arrested at a late-mature stage. Also, the population included a large subpopulation of Tregs expressing IL-7Rα, which is a possible marker of late-mature Tregs. Finally, TA-KO fetal liver chimeric mice developed an Nrp1+ splenic Treg population from TA-KO cells, suggesting that Treg arrest is caused by a lack of RelA in the thymic environment. Together, these results suggest that egress of mature Tregs from the thymus depends on RelA in the thymic environment. For the isolation of thymic Tregs, CD4+CD8α-CD25hi thymocytes were isolated from five 1.5- to 2-week-old TNFα-KO or TA-KO mice by using a FACSAria cell sorter. For the isolation of thymic stromal cells, 10 thymi from 1.5- to 2-week-old TNFα-KO or TA-KO mice were minced with scissors and treated with RPMI 1640 supplemented with 2% FCS, 0.2 mg/ml collagenase (Roche, Basel, Switzerland), 0.2 mg/ml dispase I (Roche), and 100 U/ml DNase I (Life Technologies) for 30 min with stirring. Digested thymi were centrifuged in a Percoll (GE Healthcare Bio-Sciences, Piscataway, NJ, USA) gradient (density, 1.115, 1.065, and PBS) at 1400g for 30 min. Cells in the upper layer were collected, and the CD45-EpCAM+ (thymic epithelial cells) and CD45+EpCAM- populations (enriched thymic stromal cells containing macrophages or dendritic cells) were sorted.
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Project description:Microarray analyses were performed in order to determine the effect of galectin-3 ablation on the endothelial transcriptional response in a mouse model of type 2 diabetes. Galectin-3-deficient mice (KO) and wild-type C57BL/6 (WT) were fed a high-fat diet (60% fat calories) or standard chow for 8 weeks. CD105+/CD45- endothelial cells were isolated from the aortae and skeletal muscles of these mice by FACS. Whole genome microarray expression profiling revealed greater transcriptional dysregulation in the endothelium of the KO after high-fat feeding compared to WT. Transcripts dysregulated in the KO endothelium after HFD include those involved in glucose uptake and insulin signaling, oxidative stress, vasoregulation, coagulation, and atherogenesis. Real-time PCR confirmed transcriptional downregulation of the glucose transporter, Glut4, and immunofluorescence staining confirmed reduced GLUT4 protein in the endothelium and mudcle of the KO compared to WT. The transcriptional and histological data was consistent with physiological studies showing exacerbated hyperglycemia and coagulation in the KO. These results suggest that galectin-3 serves a protective role against metabolic dysregulation and endothelial dysfunction in diabetes. Galectin-3-deficient mice (KO) and wild-type C57BL/6 (WT) were fed either a high-fat diet (60% fat calories) or standard chow diet (12% fat calories) for 8 weeks. Three independent experiments were performed. For each experiment, the aorta and skeletal muscle from 3-4 animals per diet/genotype group were excised and pooled for each tissue. Live, CD105+/CD45- endothelial cells were isolated from the aortic and muscle suspensions by FACS.
2015-08-01 | E-GEOD-57329 | biostudies-arrayexpress
Project description:The first aim was to identify genes whose transcription is induced by rapamycin feeding in Drosophila S2 cells. Secondly, the goal was to find out which contribution the transcription factors REPTOR (=CG13624) and REPTOR-BP (REPTOR-binding partner, =CG18619) has to the observed changes in expression. We thus compared gene epxression between rapamycin and control treated S2 cells in GFP, REPTOR or REPTOR-BP knockdown cells. 3 biological replicates from control knockdown plus/minus rapamycin and REPTOR knockdown plus/minus rapamycin; 2 biological replicates from REPTOR-BP knockdown cells plus/minus rapamycin; together those are 16 samples
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