E-GEOD-1491
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA90811
PROVIDER: E-GEOD-1491 | ExpressionAtlas | 2014-07-03
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-1491-analysis-methods.tsv | Tabular | |||
| E-GEOD-1491-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-1491-configuration.xml | Xml | |||
| E-GEOD-1491-percentile-ranks.tsv | Tabular | |||
| E-GEOD-1491-zoomifications-log.tsv | Tabular |
Items per page: 5 1 - 5 of 121 |
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Project description:Identification of Inhibitors of Auxin Transcriptional Activation via Chemical Genetics in Arabidopsis
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Project description:Transcriptional profiling of Arabidopsis thaliana seedlings treated with auxin (indole-3-acetic acid), highlighting to the physiological function of auxin by observing early response of gene expressions in Arabidopsis seedlings.
2012-05-10 | GSE37899 | GEO
Project description:Transcriptional profiling of Arabidopsis thaliana seedlings treated with auxin (indole-3-acetic acid), highlighting to the physiological function of auxin by observing early response of gene expressions in Arabidopsis seedlings. Two-condition experiment, auxin-treated seedlings vs. control seedlings. Biological replicates:2 control replicates, 2 auxin-treated.
2012-05-09 | E-GEOD-37899 | biostudies-arrayexpress
Project description:Canonical auxin signalling starts with auxin binding to the receptor complex, followed by modulation of gene transcription and protein abundance (Tan et al., 2007; Chapman and Estelle, 2009; Slade et al., 2017). However, recent studies also showed an alternative mechanism in roots involving intra-cellular auxin perception, but not transcriptional reprogramming (Fendrych et al., 2018). Despite knowledge on effects of auxin on Arabidopsis root growth at the protein and phosphorylation level is increasing (Zhang et al., 2013; Mattei et al., 2013; Slade et al., 2017), it still remains incomplete. To address this gap in our knowledge, we explored the impact of auxin on the root tip proteome and phosphoproteome.
2021-09-09 | PXD021267 | Pride
Project description:To obtain more information on auxin-regulated gene expression, we treated Arabidopsis seedlings with auxin biosynthesis or signaling inhibitors, then performed DNA microarray analyses.
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Project description:<p>The genetic basis of hypodiploid acute lymphoblastic leukemia (ALL), a subtype of ALL characterized by aneuploidy and poor outcome, is unknown. Genomic profiling of 124 hypodiploid ALL cases, including whole-genome and exome sequencing of 40 cases, identified two subtypes that differ in the severity of aneuploidy, transcriptional profiles and submicroscopic genetic alterations. Near-haploid ALL with 24-31 chromosomes harbor alterations targeting receptor tyrosine kinase signaling and Ras signaling (71%) and the lymphoid transcription factor gene IKZF3 (encoding AIOLOS; 13%). In contrast, low-hypodiploid ALL with 32-39 chromosomes are characterized by alterations in TP53 (91.2%) that are commonly present in nontumor cells, IKZF2 (encoding HELIOS; 53%) and RB1 (41%). Both near-haploid and low-hypodiploid leukemic cells show activation of Ras-signaling and phosphoinositide 3-kinase (PI3K)-signaling pathways and are sensitive to PI3K inhibitors, indicating that these drugs should be explored as a new therapeutic strategy for this aggressive form of leukemia.</p>
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Project description:Discovery of novel auxin-responsive genes of Arabidopsis using auxin inhibitors
| PRJNA248731 | ENA
Project description:A mutant screen was conducted in Arabidopsis that was based on deregulated expression of auxin-responsive transgenes. Two different tightly regulated (i.e., very low expression in the absence of auxin treatment and very high expression after exogenous auxin treatment) auxin-responsive promoters were used to drive the expression of both a ?-glucuronidase (GUS) reporter gene and a hygromycin phosphotransferase (HPH)?selectable marker gene. This screen yielded several mutants, and five of the mutations (axe1-1 to axe1-5) mapped to the same locus on chromosome 5. A map-based cloning approach was used to locate the axe1 mutations in an Arabidopsis RPD3-like histone deacetylase gene, referred to as HDA6. The axe1 mutant plants displayed increased expression of the GUS and HPH transgenes in the absence of auxin treatment and increased auxin-inducible expression of the transgenes compared with nonmutant control plants. None of a variety of endogenous, natural auxin-inducible genes in the mutant plants were upregulated like the transgenes, however. Results of treatment with the DNA methylation inhibitor 5-aza-2'-deoxycytidine suggest that the axe1 mutations affect transgene silencing; however, histone deacetylase inhibitors had no affect on transgene silencing in mutant or control plants. The specific effect of AtHDA6 mutations on the auxin-responsive transgenes implicates this RPD3-like histone deacetylase as playing a role in transgene silencing. Furthermore, the effect of AtHDA6 on transgene silencing may be independent of its histone deacetylase activity. *
2007-05-04 | E-SMDB-4012 | biostudies-arrayexpress
Project description:The phytohormone auxin controls a myriad of processes in plants, at least in part through its regulation of cell expansion. The "acid growth hypothesis" has been proposed to explain auxin-stimulated cell expansion for five decades, but the mechanism underlying auxin-induced cell wall acidification is poorly characterized. Auxin induces the phosphorylation and activation of the plasma membrane (PM) H+-ATPase that pumps protons into the apoplast, yet how auxin activates its phosphorylation remains elusive. Here, we show that the transmembrane kinase (TMK) auxin signaling proteins interact with PM H+-ATPases and activate their phosphorylation to promote cell wall acidification and hypocotyl cell elongation in Arabidopsis. Auxin induced TMK's interaction with H+-ATPase on the plasma membrane within 1-2 minutes as well as TMK-dependent phosphorylation of the penultimate Thr residue. Genetic, biochemical, and molecular evidence demonstrates that TMKs directly phosphorylate PM H+-ATPase and are required for auxin-induced PM H+-ATPase activation, apoplastic acidification, and cell expansion. Thus, our findings reveal a crucial connection between auxin and PM H+-ATPase activation in regulating apoplastic pH changes and cell expansion via TMK-based cell surface auxin signaling.
2021-07-14 | MSV000087822 | MassIVE
Project description:A mutant screen was conducted in Arabidopsis that was based on deregulated expression of auxin-responsive transgenes. Two different tightly regulated (i.e., very low expression in the absence of auxin treatment and very high expression after exogenous auxin treatment) auxin-responsive promoters were used to drive the expression of both a ?-glucuronidase (GUS) reporter gene and a hygromycin phosphotransferase (HPH)?selectable marker gene. This screen yielded several mutants, and five of the mutations (axe1-1 to axe1-5) mapped to the same locus on chromosome 5. A map-based cloning approach was used to locate the axe1 mutations in an Arabidopsis RPD3-like histone deacetylase gene, referred to as HDA6. The axe1 mutant plants displayed increased expression of the GUS and HPH transgenes in the absence of auxin treatment and increased auxin-inducible expression of the transgenes compared with nonmutant control plants. None of a variety of endogenous, natural auxin-inducible genes in the mutant plants were upregulated like the transgenes, however. Results of treatment with the DNA methylation inhibitor 5-aza-2'-deoxycytidine suggest that the axe1 mutations affect transgene silencing; however, histone deacetylase inhibitors had no affect on transgene silencing in mutant or control plants. The specific effect of AtHDA6 mutations on the auxin-responsive transgenes implicates this RPD3-like histone deacetylase as playing a role in transgene silencing. Furthermore, the effect of AtHDA6 on transgene silencing may be independent of its histone deacetylase activity. A replicate experimental design type is where a series of replicates are performed to evaluate reproducibility or as a pilot study to determine the appropriate number of replicates for a subsequent experiments. Computed
2007-08-09 | E-GEOD-7587 | biostudies-arrayexpress