E-GEOD-51162
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA221371PRJNA221372PRJNA221370
PROVIDER: E-GEOD-51162 | ExpressionAtlas | 2014-12-05
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-51162-analysis-methods.tsv | Tabular | |||
| E-GEOD-51162-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-51162-configuration.xml | Xml | |||
| E-GEOD-51162-percentile-ranks.tsv | Tabular | |||
| E-GEOD-51162.condensed-sdrf.tsv | Tabular |
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Similar Datasets
Project description:Genome maintenance defects cause complex disease phenotypes characterized by developmental failure, cancer susceptibility and premature aging. It remains poorly understood how DNA damage responses function during organismal development and maintain tissue functionality when DNA damage accumulates with aging. Here we show that the FoxO transcription factor DAF-16 is activated in response to DNA damage during development while the DNA damage responsiveness of DAF-16 declines with aging. We find that in contrast to its established role in mediating starvation arrest, DAF-16 alleviates DNA damage induced developmental arrest and even in the absence of DNA repair promotes developmental growth and enhances somatic tissue functionality. We demonstrate that the GATA transcription factor EGL-27 co-regulates DAF-16 target genes in response to DNA damage and together with DAF-16 promotes developmental growth. We propose that EGL-27/GATA activity specifies DAF-16 mediated DNA damage responses to enable developmental progression and to prolong tissue functioning when DNA damage persists. Synchronized L1 and mutant larvae were UV or mock treated, or starved. Mock treated samples served as controls for both the UV-treated and starved groups.
2014-11-18 | E-GEOD-51162 | biostudies-arrayexpress
Project description:Genome maintenance defects cause complex disease phenotypes characterized by developmental failure, cancer susceptibility and premature aging. It remains poorly understood how DNA damage responses function during organismal development and maintain tissue functionality when DNA damage accumulates with aging. Here we show that the FoxO transcription factor DAF-16 is activated in response to DNA damage during development while the DNA damage responsiveness of DAF-16 declines with aging. We find that in contrast to its established role in mediating starvation arrest, DAF-16 alleviates DNA damage induced developmental arrest and even in the absence of DNA repair promotes developmental growth and enhances somatic tissue functionality. We demonstrate that the GATA transcription factor EGL-27 co-regulates DAF-16 target genes in response to DNA damage and together with DAF-16 promotes developmental growth. We propose that EGL-27/GATA activity specifies DAF-16 mediated DNA damage responses to enable developmental progression and to prolong tissue functioning when DNA damage persists. Synchronized L1 and xpa-1 mutant larvae were UV or mock treated, or starved
2014-11-18 | E-GEOD-51161 | biostudies-arrayexpress
Project description:This experiment was designed to identify early targets of daf-16/FoxO during L1 starvation in C. elegans. Previous work (Baugh et al 2009) examined temporal dynamics of gene expression in fed and starved L1 larvae using the same platform and methods. Here, a single time point was analyzed (~3 hr after hatching) in fed and starved larvae also comparing wild-type and a daf-16 null mutant. Statistical analysis includes pairwise comparisons between the four conditions as well as a two-factor analysis to explicitly identify genes affected by nutrient availability in daf-16-dependent fashion.
2017-05-24 | GSE99201 | GEO
Project description:Cell lines B2B and 16HBE were infected in-vitro with rhinovirus 16 and comparisons were made to mock-infected cultures and cultures exposed to UV-irradiated rhinovirus. Total RNA were extracted and assessed by whole genome expression arrays.
2014-04-01 | GSE28904 | GEO
Project description:Post-embryonic development of the nematode C. elegans is governed by nutrient availability. L1-stage larvae remain in a state of developmental arrest after hatching until they feed. This “L1 arrest” (or "L1 diapause") is associated with increased stress resistance, supporting starvation survival. Loss of the transcription factor daf-16/FOXO, an effector of insulin/IGF signaling, results in arrest-defective and starvation-sensitive phenotypes. We show that daf-16/FOXO regulates L1 arrest cell-nonautonomously, suggesting that insulin/IGF signaling regulates at least one additional signaling pathway. We used mRNA-seq to identify candidate signaling molecules affected by daf-16/FOXO during L1 arrest. daf-16/FOXO had overlapping but distinct effects on gene expression in L1 arrest compared to daf-2/InsR adults. Notably, dbl-1/TGF-β, a ligand for the Sma/Mab pathway, and daf-36, which encodes an upstream component of the daf-12/NHR steroid hormone signaling pathway, were up-regulated during L1 arrest in a daf-16/FOXO mutant. Using genetic epistasis analysis, we show that dbl-1/TGF-β and daf-12/NHR steroid hormone signaling pathways are required for the daf-16/FOXO arrest-defective phenotype, suggesting that daf-16/FOXO represses dbl-1/TGF-β and daf-36. The dbl-1/TGF-β and daf-12/NHR pathways have not previously been shown to affect L1 development, but we found that disruption of these pathways delayed L1 development in fed larvae, consistent with these pathways promoting development in starved daf-16/FOXO mutants. Though the dbl-1/TGF-β and daf-12/NHR pathways are epistatic to daf-16/FOXO for the arrest-defective phenotype, disruption of these pathways does not suppress starvation sensitivity of daf-16/FOXO mutants. This observation uncouples starvation survival from developmental arrest, indicating that DAF-16/FOXO targets distinct effectors for each phenotype, and revealing that inappropriate development during starvation does not cause the early demise of daf-16/FOXO mutants. Overall, this study shows that daf-16/FOXO promotes developmental arrest cell-nonautonomously by repressing pathways that promote larval development.
2016-05-27 | GSE69329 | GEO
Project description:Transcription profiling by array of maize ears infected with Sporisorium reilianum for 4 weeks against mock-infected controls
2016-10-04 | E-GEOD-29747 | ExpressionAtlas
Project description:In this study we have investigated the effect of loss of math-33 activity on DAF-16-mediated target gene regulation in C. elegans under conditions of reduced Insulin/IGF-1 signaling (IIS). Using whole nematode RNA sequencing experiments we found that the daf-2(e1370)-mediated induction and repression of DAF-16 target genes was decreased in daf-2(e1370); math-33(tm3561) mutant animals. Our data suggest that the downregulation of endogenous DAF-16 isoforms in the absence of a functional MATH-33 severely affects the global expression of DAF-16 targets when IIS activity is reduced. Therefore, MATH-33 is essential for DAF-16-mediated target gene activation and repression in the context of IIS. DAF-16 mediated target gene regulation was analyzed in daf-2(e1370) nematodes and compared to daf-2(e1370); math-33(tm3561) mutant animals. daf-16(mu86); daf-2(e1370); N2 (wild type) and math-33(tm3561) single mutant animals were used as controls.
2016-06-22 | E-GEOD-70117 | biostudies-arrayexpress
Project description:We confirmed that the life span of C. elegans feeding hns mutant E. coli was increased. hns mutant E. coli was found to regulate lifespan of C. elegans through daf-16 activation in C. elegans. It is well known that daf-16 is the transcription factor of the insulin/IGF-1 signaling pathway and it is known to regulate downstream genes such as longevity, stress response, and dauer diapause regulation genes. Thus, we performed Next Generation Sequencing(NGS) to investigate the downstream genes regulated by daf-16 in C. elegans that are activated by hns mutant E. coli. N2 wild type worms and daf-16 mutant worms were fed with BW25113 wild type E. coli and hns mutant E. coli, respectively, and then NGS was performed by harvesting the worms and purifying the RNA. We investigated how the downstream genes of daf-16 of C. elegans, which is regulated by hns mutant E. coli, differs from the downstream genes of daf-16 of C. elegans, which is regulated by the insulin/IGF-1 signaling pathway. To do this, we carried out the analysis including two previous studied papers that analyzed the daf-16 downstream genes related to the insulin/IGF-1 signaling pathway. Surprisingly, only 6 genes were up-regulated in all three experiments and 288 genes were found to be dependent on daf-16 and hns mutant E. coli. This study indicated that hns mutant E. coli regulate daf-16 distinct from insulin/IGF-1 signaling pathway on C. elegans.
2020-07-29 | GSE114160 | GEO
Project description:Transcription profiling by array of maize leaves 36 and 96 hours after infection with fungal pathogen Colletotrichum graminicola against mock controls
2016-10-04 | E-GEOD-31188 | ExpressionAtlas
Project description:Transcriptional profiling of Zea mays roots infected by necrotrophic pathogen Phytophthora cinnamomi for 6 or 24 hours against mock-infected controls
2016-10-04 | E-GEOD-27626 | ExpressionAtlas