E-GEOD-53824
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-53824 | ExpressionAtlas | 2016-12-08
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-53824-analysis-methods.tsv | Tabular | |||
| E-GEOD-53824-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-53824-configuration.xml | Xml | |||
| E-GEOD-53824-percentile-ranks.tsv | Tabular | |||
| E-GEOD-53824.condensed-sdrf.tsv | Tabular |
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Similar Datasets
Project description:Infection by the pathogen grape powdery mildew (Erysiphe necator) causes changes in the transcriptome of its susceptible host Vitis vinifera. Infection triggers the host to synthesize the signaling molecule salicylic acid (SA) which regulates the expression of a broad range of defense-related plant genes. In addition, it is hypothesized that E. necator directly modulates gene expression in V. vinifera via the haustorial complex. This microarray experiment was designed to dissect host transcriptome changes triggered directly by E. necator infection and indirectly through the SA response. We accomplished this by conducting two separate global leaf transcriptome analyses using the Vitis Affymetrix GeneChip platform: in one, we compared the leaves with fully established PM colonies to healthy reference leaves, in another, we compared healthy leaves with artificially elevated SA levels to healthy reference leaves. Overlaying host transcriptome changes from these two experiments enabled us to glean out V. vinifera genes that modulate their expression in response E. necator in an SA-independent manner.
2014-01-10 | GSE53824 | GEO
Project description:Infection by the pathogen grape powdery mildew (Erysiphe necator) causes changes in the transcriptome of its susceptible host Vitis vinifera. Infection triggers the host to synthesize the signaling molecule salicylic acid (SA) which regulates the expression of a broad range of defense-related plant genes. In addition, it is hypothesized that E. necator directly modulates gene expression in V. vinifera via the haustorial complex. This microarray experiment was designed to dissect host transcriptome changes triggered directly by E. necator infection and indirectly through the SA response. We accomplished this by conducting two separate global leaf transcriptome analyses using the Vitis Affymetrix GeneChip platform: in one, we compared the leaves with fully established PM colonies to healthy reference leaves, in another, we compared healthy leaves with artificially elevated SA levels to healthy reference leaves. Overlaying host transcriptome changes from these two experiments enabled us to glean out V. vinifera genes that modulate their expression in response E. necator in an SA-independent manner. We characterized gene expression profiles in (1) healthy reference leaves, (2) leaves with well-established by E. necator colonies, and (3) healthy leaves in which SA levels were artificially elevated by the presence of methyl salicylate (15 µM) in the atmosphere. Treatments (1) and (2) differed only in the presence E. necator infection, whereas treatments (1) and (3) differed only in SA levels. Consequently, statistical comparisons were made only between signal intensities from treatments (1) and (2) and from treatments (1) and (3). Each treatment was done in three biological repeats, that is, each experiment was repeated three times in 14-day intervals with dedicated biological material (plants were used in a single replicate and not reused in another repeat or treatment). Each biological replicate consisted of 10 potted vines. For RNA extraction, two young leaves were harvested from each of the 10 vines and pooled into a single sample.
2014-01-10 | E-GEOD-53824 | biostudies-arrayexpress
Project description:Grape powdery mildew (PM), caused by the biotrophic ascomycete Erysiphe necator, is a devastating fungal disease that affects most Vitis vinifera cultivars. We have previously identified a panel of V. vinifera accessions from Central Asia with partial resistance to PM that possess a Ren1-like local haplotype. In this study we show that in addition to the typical Ren1-associated late post-penetration resistance, these accessions display a range of different levels of disease development suggesting that alternative alleles or additional genes contribute to determining the outcome of the interaction with the pathogen. To identify potential Ren1-dependent transcriptional responses and functions associated with the different levels of resistance, we sequenced and analyzed the transcriptomes of these Central Asian accessions at two time-points of PM infection. Transcriptomes were compared to identify constitutive differences and PM-inducible responses that may underlie their disease resistant phenotype. Responses to E. necator in all resistant accessions were characterized by an early up-regulation of 13 genes, most encoding putative defense functions, and a late down-regulation of 32 genes, enriched in transcriptional regulators and protein kinases. Potential Ren1-dependent responses included a hotspot of co-regulated genes on chromosome 18. We also identified 81 genes whose expression levels and dynamics correlated with the phenotypic differences between the most resistant accessions ?Karadzhandahal?, DVIT3351.27, and O34-16 and the other genotypes. This study provides a first exploration of the functions associated with varying levels of partial resistance to PM in V. vinifera accessions that can be exploited as sources of genetic resistance in grape breeding programs. Eight varieties (7 resistant to powdery mildew, 2 of which are V. vinifera spp. sylvestris, 5 of which are V. vinifera spp. sativa) are infected with powdery mildew (E. necator) at two timepoints (1 dpi and 5 dpi) with three replicates for each timepoint for each condition (uninfected vs. infected), for a total of 96 samples
2015-07-20 | E-GEOD-67191 | biostudies-arrayexpress
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:Study of gene expression during Plasmopara viticola infection in the resistant Vitis vinifera cultivar 'Regent'. The oomycete fungus Plasmopara viticola (Berk. et Curt.) Berl. et de Toni is responsible for grapevine downy mildew disease. Most of the cultivated grapevines are sensitive to this pathogen, thus requiring intensive fungicide treatments. The molecular basis of resistance to this pathogen is poorly understood. We have carried out a cDNA microarray transcriptome analysis to identify grapevine genes associated with resistance traits. Early transcriptional changes associated with downy mildew infection in the resistant Vitis vinifera cultivar ‘Regent’, when compared to the susceptible cultivar ‘Trincadeira’, were analyzed. Transcript levels were measured at three time-points: 0, 6 and 12 hours post inoculation (hpi). Our data indicate that resistance in V. vinifera ‘Regent’ is induced after infection. This study provides the identification of several candidate genes that may be related to ‘Regent’ defense mechanisms, allowing a better understanding of this cultivar's resistance traits.
2012-04-06 | GSE28439 | 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. Keywords: disease state comparison
2005-09-30 | GSE3220 | GEO
Project description:For transcript analysis of early hypersensitive and susceptible responses of Medicago truncatula to the powdery mildew pathogen, Erysiphe pisi, we compared transcripts from pathogen-inoculated and control (non-inoculated) plants 12 h after infection in resistant (A14), partially resistant (A20), and susceptible (DZA315.16) genotypes. Published in: Medicago truncatula to the powdery mildew 1 and anthracnose pathogens, Erysiphe pisi and Colletotrichum trifolii. Molecular Plant Pathology 8(3):307-319 Keywords: 1 time points and 3 genotypes
2007-01-25 | GSE6840 | GEO
Project description:Grape powdery mildew (PM), caused by the biotrophic ascomycete Erysiphe necator, is a devastating fungal disease that affects most Vitis vinifera cultivars. We have previously identified a panel of V. vinifera accessions from Central Asia with partial resistance to PM that possess a Ren1-like local haplotype. In this study we show that in addition to the typical Ren1-associated late post-penetration resistance, these accessions display a range of different levels of disease development suggesting that alternative alleles or additional genes contribute to determining the outcome of the interaction with the pathogen. To identify potential Ren1-dependent transcriptional responses and functions associated with the different levels of resistance, we sequenced and analyzed the transcriptomes of these Central Asian accessions at two time-points of PM infection. Transcriptomes were compared to identify constitutive differences and PM-inducible responses that may underlie their disease resistant phenotype. Responses to E. necator in all resistant accessions were characterized by an early up-regulation of 13 genes, most encoding putative defense functions, and a late down-regulation of 32 genes, enriched in transcriptional regulators and protein kinases. Potential Ren1-dependent responses included a hotspot of co-regulated genes on chromosome 18. We also identified 81 genes whose expression levels and dynamics correlated with the phenotypic differences between the most resistant accessions ?Karadzhandahal?, DVIT3351.27, and O34-16 and the other genotypes. This study provides a first exploration of the functions associated with varying levels of partial resistance to PM in V. vinifera accessions that can be exploited as sources of genetic resistance in grape breeding programs.
2015-07-20 | GSE67191 | GEO
Project description:Clubroot caused by the protist pathogen Plasmodiophora brassicae Woronin is a major disease in Brassica crops. Growing clubroot-resistant cultivars is the most effective and practical control strategy, but resistance genes can often be overcome by emerging pathotypes. In this study, we identified PMR4 as a potential host susceptibility factor that can be targeted as a novel genetic resource for durable clubroot resistance. Recessive PMR4 mutations in Arabidopsis thaliana conferred strong resistance to multiple P. brassicae pathotypes, independent of salicylic acid-mediated plant immunity. Using CRISPR/Cas9, we edited two PMR4 orthologs in the Brassica napus genome, and the resulting homozygous mutants exhibited resistance to both powdery mildew and clubroot diseases. While PMR4 is known to mediate callose deposition at wound and powdery mildew infection sites in leaves, this study reveals that P. brassicae infection induces callose deposition in Arabidopsis and B. napus roots in a PMR4-dependent manner. The Arabidopsis pmr4-1 mutation does not affect P. brassicae primary infection but blocks the pathogen entry from epidermal cells to stele in a jasmonic acid signaling-dependent manner, which is also correlated with enriched lignin-like and suberin compounds in periderm cell walls. Together, these findings establish PMR4-encoded callose synthase as a host susceptibility factor that facilitates P. brassicae secondary infection in host roots and demonstrate its potential as a gene-editing target for enhancing resistance to both powdery mildew and clubroot diseases as well as other possible biotic and abiotic stresses in Brassicaceae crops.
2026-07-01 | GSE317839 | GEO
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