E-GEOD-431
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA85005
PROVIDER: E-GEOD-431 | ExpressionAtlas | 2014-07-14
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:To explore the transcriptional regulations in pip5k1 pip5k2 mutant and wild type plants before or after inoculation with powdery mildew Erysiphe cichoracearum
2020-03-10 | GSE127919 | GEO
Project description:We performed RNA-sequencing of Golovinomyces orontii-infected Arabidopsis leaves of wild type, the double or triple mutants of AtMLKLs to examine the role of AtMLKLs in response to the powdery mildew fungus.
2019-03-29 | GSE129011 | GEO
Project description:The edr1 mutant of Arabidopsis thaliana displays enhanced resistance to the powdery mildew Golovinomyces cichoracearum, resulting in cell death and an absence of visible disease symptoms. To better characterize and understand the defense response of edr1, a time course of early signaling responses was performed after inoculation with powdery mildew and compared to the responses of wild-type Col-0. These time points represent early stages in the infection process, before any signs of susceptibility or resistance are visible. Four-week-old Col-0 and edr1 plants were inoculated with powdery mildew and whole rosettes were collected at 0, 18, 36, and 96 hours post inoculation. Each sample is a pool of four rosettes processed together.
2011-01-19 | E-GEOD-26679 | biostudies-arrayexpress
Project description:Differential expression of genes between Arabidopsis WRKY18/40 knock out and wild type plants, after 8 h post inoculation of powdery mildew pathogen.
2010-09-01 | E-MEXP-2371 | biostudies-arrayexpress
Project description:The edr1 mutant of Arabidopsis thaliana displays enhanced resistance to the powdery mildew Golovinomyces cichoracearum, resulting in cell death and an absence of visible disease symptoms. To better characterize and understand the defense response of edr1, a time course of early signaling responses was performed after inoculation with powdery mildew and compared to the responses of wild-type Col-0. These time points represent early stages in the infection process, before any signs of susceptibility or resistance are visible.
2011-01-19 | GSE26679 | GEO
Project description:There were two genotypes: (1) Columbia-0, wild-type (C) (2) pmr4-1 mutant (P), callose synthase deficient mutant (Vogel and Somerville (2000) Proc. Natl. Acad. Sci., USA 97: 1897). There were two treatments: (1) uninoculated (U) (2) 3 days after inoculation with the powdery mildew pathogen, Erysiphe cichoracearum, race UCSC (I). There were four biological replicates, labeled 1, 2, 3 or 4. Examples of the sample labels are: CU1 = Columbia-0, uninoculated, replicate 1 CI2 = Columbia-0, 3 days after inoculation with powdery mildew, replicate 2 PU3 = pmr4-1, uninoculated, replicate 3 PI4 = pmr4-1, 3 days after inoculation with powdery mildew, replicate 4. In total, there were 16 Affymetrix ATH1 GeneChips (2 genotypes x 2 treatments x 4 biological replicates). Keywords: repeat sample
2003-08-15 | GSE431 | GEO
Project description:There were two genotypes:,(1) Columbia-0, wild-type (C),(2) pmr4-1 mutant (P), callose synthase deficient mutant (Vogel and Somerville (2000) Proc. Natl. Acad. Sci., USA 97: 1897).,There were two treatments:,(1) uninoculated (U),(2) 3 days after inoculation with the powdery mildew pathogen, Erysiphe cichoracearum, race UCSC (I).,There were four biological replicates, labeled 1, 2, 3 or 4.,Examples of the sample labels are:,CU1 = Columbia-0, uninoculated, replicate 1,CI2 = Columbia-0, 3 days after inoculation with powdery mildew, replicate 2,PU3 = pmr4-1, uninoculated, replicate 3,PI4 = pmr4-1, 3 days after inoculation with powdery mildew, replicate 4.,In total, there were 16 Affymetrix ATH1 GeneChips (2 genotypes x 2 treatments x 4 biological replicates).
2007-07-13 | E-GEOD-431 | biostudies-arrayexpress
Project description:Arabidopsis does not support the growth and asexual reproduction of the barley pathogen, Blumeria graminis f. sp. hordei Bgh). A majority of germlings fail to penetrate the epidermal cell wall and papillae. To gain additional insight into this interaction, we determined whether the salicylic acid (SA) or jasmonate (JA)/ethylene (ET) defence pathways played a role in blocking barley powdery mildew infections. Only the eds1 mutant and NahG transgenics supported a modest increase in penetration success by the barley powdery mildew. We also compared the global gene expression patterns of Arabidopsis inoculated with the non-host barley powdery mildew to those inoculated with a virulent, host powdery mildew, Erysiphe cichoracearum. Genes repressed by inoculations with non-host and host powdery mildews relative to non-inoculated control plants accounted for two-thirds of the differentially expressed genes. A majority of these genes encoded components of photosynthesis and general metabolism. Consistent with this observation, Arabidopsis growth was inhibited following inoculation with Bgh, suggesting a shift in resource allocation from growth to defence. A number of defence-associated genes were induced during both interactions. These genes likely are components of basal defence responses, which do not effectively block host powdery mildew infections. In addition, genes encoding defensins, anti-microbial peptides whose expression is under the control of the JA/ET signalling pathway, were induced exclusively by non-host pathogens. Ectopic activation of JA/ET signalling protected Arabidopsis against two biotrophic host pathogens. Taken together, these data suggest that biotrophic host pathogens must either suppress or fail to elicit the JA/ET signal transduction pathway. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs
2005-08-26 | GSE3199 | GEO
Project description:Arabidopsis is a host to the fungal powdery mildew pathogen, Erysiphe cichoracearum, and a nonhost to Blumeria graminis f.sp. hordei, the powdery mildew pathogenic on barley. A screen for mutants that allowed increased entry by this inappropriate or nonhost pathogen on Arabidopsis led to the identification of PEN3. While pen3 mutants permitted both increased penetration and increased hyphal growth by B. g. hordei, they were unexpectedly resistant to E. cichoracearum. This resistance was correlated with the appearance of chlorotic patches and was salicylic acid-dependent. Consistent with this observation, microarray analysis revealed that the salicylic acid defense pathway was hyper-induced in pen3 relative to wild type following inoculation with either E. cichoracearum or B. g. hordei. The pen3 phenotypes result from a loss of function of AtPDR8, a ubiquitously and highly expressed ATP binding cassette transporter. PEN3 protein tagged with green fluorescent protein localized to the plasma membrane in uninfected cells. In infected leaves, the protein concentrated to high levels at infection sites and surrounded fungal penetration pegs. We hypothesize that PEN3 may be involved in exporting toxic substrates to sites of infection and that accumulation of these substrates intracellularly in the pen3 mutant may secondarily activate the salicylic acid pathway. Experiment Overall Design: Three week-old wild-type Col and mutant pen3 Arabidopsis thaliana plants were inoculated with Erysiphe cichoracearum, Blumeria graminis hordei, or not inoculated. 1 day post inoculation 16 rosettes were harvested per replicate. 4 replicates were perfomerd per treatment.
2007-10-04 | E-GEOD-3220 | biostudies-arrayexpress
Project description:In plants, the activation of immunity is often inversely correlated with growth. Mechanisms that plant growth in the context of pathogen challenge and immunity are unclear. Investigating Arabidopsis infection with the powdery mildew fungus, we find that the Arabidopsis atypical E2F DEL1, a transcriptional repressor known to promote cell proliferation, represses accumulation of the hormone salicylic acid (SA), an established regulator of plant immunity. DEL1 deficient plants are more resistant to pathogens and slightly smaller than wild type. The resistance and size phenotypes of DEL1 deficient plants are due to the induction of SA and activation of immunity in the absence of pathogen challenge. Moreover, Enhanced Disease Susceptibility 5 (EDS5), a SA transporter required for elevated SA and immunity, is a direct repressed target of DEL1. Together, these findings indicate that DEL1 control of SA levels contributes to regulating the balance between growth and immunity in developing leaves.
2014-04-30 | GSE40973 | GEO