Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1043471 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26897268_1.fastq.gz | Fastqsanger.gz | |||
| SRR26897268_2.fastq.gz | Fastqsanger.gz | |||
| SRR26897269_1.fastq.gz | Fastqsanger.gz | |||
| SRR26897269_2.fastq.gz | Fastqsanger.gz | |||
| SRR26897270_1.fastq.gz | Fastqsanger.gz |
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Project description:A comparison of the transcriptomes of wild type Cochliolobolus heterostrophus and a deletion mutant in the redox-sensing transcription factor ChAP1 was made. The aim was to study the role of ChAP1 in the response of this pathogen of maize to exposure to a plant-derived phenolic
2019-01-18 | GSE125235 | GEO
Project description:Studies investigating crop resistance to biotic and abiotic stress have largely focused on plant responses to singular forms of stress and individual biochemical pathways that only partially represent stress responses. Thus, combined biotic and abiotic stress treatments and the global assessment of their elicited metabolic expression remains largely unexplored. In this study, we employed targeted and untargeted metabolomics to investigate the metabolic responses of maize (Zea mays) to both individual and combinatorial stress treatments using heat (abiotic) and Cochliobolus heterostrophus infection (biotic) experiments. Ultra-high-performance liquid chromatography-high-resolution mass spectrometry revealed significant metabolic responses to C. heterostrophus infection and heat stress, and comparative analyses between these individual forms of stress demonstrated differential elicitation between the two global metabolomes. In combinatorial experiments, treatment with heat stress prior to fungal inoculation negatively impacted maize disease resistance against C. heterostrophus, and distinct metabolome separation between combinatorial stressed plants and the non-heat stressed infected controls was observed. Targeted analysis revealed inducible primary and secondary metabolite responses to biotic/abiotic stress, and combinatorial experiments indicated that deficiency in the hydroxycinnamic acid, p-coumaric acid, may lead to the heat-induced susceptibility of maize to C. heterostrophus. Collectively, these findings demonstrate that abiotic stress can predispose crops to more severe disease symptoms, underlining the increasing need to investigate defense chemistry in plants under combinatorial stress.
2020-08-03 | ST001489 | MetabolomicsWorkbench
Project description:Plant damage promotes the interaction of lipoxygenases (LOX) with fatty acids yielding 9-hydroperoxides, 13-hydroperoxides and complex arrays of oxylipins. The action of 13-LOX on linolenic acid enables production of 12-oxo-phytodienoic acid (12-OPDA) and its downstream products, termed jasmonates. As signals, jasmonates have related yet distinct roles in the regulation of plant resistance against insect and pathogen attack. A similar pathway involving 9-LOX activity on linolenic and linoleic acid leads to the 12-OPDA positional isomer, 10-oxo-11-phytodienoic acid (10-OPDA) and 10-oxo-11-phytoenoic acid (10-OPEA), respectively; however, physiological roles for 9-LOX cyclopentenones have remained unclear. In developing maize (Zea mays) leaves, southern leaf blight (Cochliobolus heterostrophus) infection results in dying necrotic tissue and the localized accumulation of 10-OPEA, 10-OPDA and a series of related 14- and 12-carbon metabolites, collectively termed ‘death acids’. 10-OPEA accumulation becomes wound-inducible within fungal-infected tissues and at physiologically relevant concentrations acts as a phytoalexin by suppressing the growth of fungi and herbivores including Aspergillus flavus, Fusarium verticillioides, and Helicoverpa zea. Unlike previously established maize phytoalexins, 10-OPEA and 10-OPDA display significant phytotoxicity. Both 12-OPDA and 10-OPEA promote the transcription of defense genes encoding glutathione S-transferases, cytochrome P450s, and pathogenesis-related proteins. In contrast, 10-OPEA only weakly promotes the accumulation of multiple protease inhibitor transcripts. Consistent with a role in dying tissue, 10-OPEA application promotes cysteine protease activation and cell death which is inhibited by overexpression of the cysteine protease inhibitor maize cystatin-9. Functions for 10-OPEA and associated death acids are consistent with specialized roles in local defense reactions. A total of 6 samples were analyzed, comprised of two treatments: 10-OPEA and DMSO carrier control (5%DMSO/0.1% Tween20 in H20), both in replicates of three.
2015-08-07 | E-GEOD-69659 | biostudies-arrayexpress
Project description:Plant damage promotes the interaction of lipoxygenases (LOX) with fatty acids yielding 9-hydroperoxides, 13-hydroperoxides and complex arrays of oxylipins. The action of 13-LOX on linolenic acid enables production of 12-oxo-phytodienoic acid (12-OPDA) and its downstream products, termed jasmonates. As signals, jasmonates have related yet distinct roles in the regulation of plant resistance against insect and pathogen attack. A similar pathway involving 9-LOX activity on linolenic and linoleic acid leads to the 12-OPDA positional isomer, 10-oxo-11-phytodienoic acid (10-OPDA) and 10-oxo-11-phytoenoic acid (10-OPEA), respectively; however, physiological roles for 9-LOX cyclopentenones have remained unclear. In developing maize (Zea mays) leaves, southern leaf blight (Cochliobolus heterostrophus) infection results in dying necrotic tissue and the localized accumulation of 10-OPEA, 10-OPDA and a series of related 14- and 12-carbon metabolites, collectively termed ‘death acids’. 10-OPEA accumulation becomes wound-inducible within fungal-infected tissues and at physiologically relevant concentrations acts as a phytoalexin by suppressing the growth of fungi and herbivores including Aspergillus flavus, Fusarium verticillioides, and Helicoverpa zea. Unlike previously established maize phytoalexins, 10-OPEA and 10-OPDA display significant phytotoxicity. Both 12-OPDA and 10-OPEA promote the transcription of defense genes encoding glutathione S-transferases, cytochrome P450s, and pathogenesis-related proteins. In contrast, 10-OPEA only weakly promotes the accumulation of multiple protease inhibitor transcripts. Consistent with a role in dying tissue, 10-OPEA application promotes cysteine protease activation and cell death which is inhibited by overexpression of the cysteine protease inhibitor maize cystatin-9. Functions for 10-OPEA and associated death acids are consistent with specialized roles in local defense reactions.
2015-08-07 | GSE69659 | GEO
Project description:The CPS1 gene was identified as a virulence factor in the maize pathogen, Cochliobolus heterostrophus. Hypothesizing that the homologous gene in Coccidioides posadasii (Cp) could be important for virulence, we created a deletion mutant, Îcps1, which was unable to cause disease in three strains of mice (C57BL/6, BALB/c, or the severely immunodeficient NOD-scid,γcnull [NSG]). Only a single colony was recovered from one of 60 C57BL/6 mice following intranasal infections of up to 4400 spores. Following administration of very high doses (10,000 to 2.5 x 10^7 spores) to NSG and BALB/c mice, spherules were observed in lung sections at time points from day 3 to day 10 post-infection, but nearly all appeared degraded with infrequent endosporulation. Although the role of CPS1 in virulence is not understood, phenotypic alterations and transcription differences of at least 33 genes in Îcps1 vs. Cp is consistent with both metabolic and regulatory functions for the gene. The in vitro phenotype of Îcps1 showed slower growth of mycelia with delayed and lower spore production compared to Cp, and in vitro spherules were smaller. Vaccination of C57BL/6 or BALB/c mice with live Îcps1 spores either intranasally, intraperitoneally or subcutaneously resulted in over 95% survival with mean residual lung fungal burdens <1000 colony-forming units from an otherwise lethal Cp intranasal infection. Considering its apparently complete attenuation of virulence and the high degree of resistance to Cp infection when used as a vaccine, Îcps1 is a promising vaccine candidate for preventing coccidioidomycosis in humans or other animals. Wild type and CPS1 deletion mutant strains of Coccidioides posadasii strain Silveira spherules grown for 48 hours in Converse medium at 38 degrees celsius in duplicate. RNAseq was performed on an Illumina HiSeq2000 (2x100 paired end).
2016-08-15 | E-GEOD-85364 | biostudies-arrayexpress
Project description:The CPS1 gene was identified as a virulence factor in the maize pathogen, Cochliobolus heterostrophus. Hypothesizing that the homologous gene in Coccidioides posadasii (Cp) could be important for virulence, we created a deletion mutant, Δcps1, which was unable to cause disease in three strains of mice (C57BL/6, BALB/c, or the severely immunodeficient NOD-scid,γcnull [NSG]). Only a single colony was recovered from one of 60 C57BL/6 mice following intranasal infections of up to 4400 spores. Following administration of very high doses (10,000 to 2.5 x 10^7 spores) to NSG and BALB/c mice, spherules were observed in lung sections at time points from day 3 to day 10 post-infection, but nearly all appeared degraded with infrequent endosporulation. Although the role of CPS1 in virulence is not understood, phenotypic alterations and transcription differences of at least 33 genes in Δcps1 vs. Cp is consistent with both metabolic and regulatory functions for the gene. The in vitro phenotype of Δcps1 showed slower growth of mycelia with delayed and lower spore production compared to Cp, and in vitro spherules were smaller. Vaccination of C57BL/6 or BALB/c mice with live Δcps1 spores either intranasally, intraperitoneally or subcutaneously resulted in over 95% survival with mean residual lung fungal burdens <1000 colony-forming units from an otherwise lethal Cp intranasal infection. Considering its apparently complete attenuation of virulence and the high degree of resistance to Cp infection when used as a vaccine, Δcps1 is a promising vaccine candidate for preventing coccidioidomycosis in humans or other animals.
2016-08-15 | GSE85364 | GEO
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