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PROVIDER: PRJNA897013 | ENA |
REPOSITORIES: ENA
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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: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: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: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: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:Powdery mildew (Erysiphe necator) is a widespread and economically important disease of grapevines. Large quantities of fungicides are used for its control, accelerating the incidence of fungicide-resistance. A shotgun approach was applied to sequence and assemble the E. necator genome of five isolates, and RNA-seq and comparative genomics were used to predict and annotate protein-coding genes. In addition, a collection of 98 E. necator isolates collected from diverse locations was used for SSR profiling and was screened for copy number variation and presence/absence of a single point mutation (Y136F) in the CYP51 gene, a key target for DMI fungicides. Our results show that the E. necator genome is exceptionally large and repetitive and suggests that transposable elements are responsible for genome expansion. Frequent structural variations were found between isolates and included copy number variant (CNV) in CYP51. We show that CYP51 copy number correlates with expression level and that an increase in copy number is detected in isolates collected from fungicide-treated vineyards. This copy number variation was usually detected with the CYP51 mutant allele (Y136F), suggesting that an increase in copy number becomes advantageous only when the allele is mutated. We also show that CYP51 copy number correlates with fungal growth in the presence of DMI fungicide in vitro. These results suggest that copy number variation can be adaptive in the development of resistance to DMI fungicides in E. necator. Detach Carignan leaves were sprayed with a Erysiphe necator C-strain conida suspension, leaves were collected in 4 time points (12 hours, 24 hours, 3 days, and 6 days) post inoculation. For each time point, two leaves from the same seedling were pooled and frozen in liquid nitrogen, and each time point was performed in triplicate.
2014-12-10 | E-GEOD-58958 | biostudies-arrayexpress
Project description:Powdery mildew (Erysiphe necator) is a widespread and economically important disease of grapevines. Large quantities of fungicides are used for its control, accelerating the incidence of fungicide-resistance. A shotgun approach was applied to sequence and assemble the E. necator genome of five isolates, and RNA-seq and comparative genomics were used to predict and annotate protein-coding genes. In addition, a collection of 98 E. necator isolates collected from diverse locations was used for SSR profiling and was screened for copy number variation and presence/absence of a single point mutation (Y136F) in the CYP51 gene, a key target for DMI fungicides. Our results show that the E. necator genome is exceptionally large and repetitive and suggests that transposable elements are responsible for genome expansion. Frequent structural variations were found between isolates and included copy number variant (CNV) in CYP51. We show that CYP51 copy number correlates with expression level and that an increase in copy number is detected in isolates collected from fungicide-treated vineyards. This copy number variation was usually detected with the CYP51 mutant allele (Y136F), suggesting that an increase in copy number becomes advantageous only when the allele is mutated. We also show that CYP51 copy number correlates with fungal growth in the presence of DMI fungicide in vitro. These results suggest that copy number variation can be adaptive in the development of resistance to DMI fungicides in E. necator.
2014-12-10 | GSE58958 | GEO
Project description:Powdery mildew caused by Erysiphe cruciferarum, is an epidemic of oil rapeseed (Brassica napus) growing worldwide, but resistant germplasm is rare in this species. We obtained the hybrid seeds of distant hybridization between powdery-mildew-immune Brassica carinata cultivar ‘White flower’ and susceptible B. napus cultivar ‘Zhongshuang11’. Five lines in the BC1F3 generation (F3 after backcross to 'Zhongshuang11') were identified to be resistant or moderately resistant. In order to identify the important biological responses to powdery mildew, the foliar transcriptomes of the resistant and susceptible plants in these progenies after powdery mildew inoculation were compared by using Illumina RNA-seq. We identified 10,454 differential expression genes (DEGs) and 1050 genes out of them are related to disease resistance. There were 271 DEGs in Group Resistance expressed at least two fold higher than in group S, while 779 DGEs expressed two fold lower. The genes highly expressed in Group Resistance are those encoding the proteins: (1) related to wax, chloroplast and cell wall metabolism, such as KCS6, CSP41B, RWA, callose synthetase 3, pectinase 9, fructosidase 2, 9s-lipoxygenase LOX2, etc.; (2) kinases including RKL, ERECTA, BAK1, BAM2, LysM receptor like kinase, and lipid transfer protein kinase ERl1 and ERl2; (3) broad spectrum powdery mildew resistance proteins RPW8, calmodulin MLO2, PMR5, MLP328, EDR2, RPS4 and RPS6, etc. In group susceptible, pectinesterase, cytochrome CYP81f2, LOX1, cysteine rich receptor protein kinases and serine / threonine protein kinases such as MEKK, RLK6, CRK45, APK1, BRl3, WAK1, WAK10, etc., and TIR-NB-LRR receptor like proteins R1M1, DSC1, DSC2 and pathogenesis-related protein PR-1 etc. were the most activated genes. The results provide the preliminarily knowledge about molecular mechanism in rapeseed defense response to powdery mildew.
2021-11-11 | GSE188377 | 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: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