Transcriptomic study of the response of the maize pathogen Cochliobolus heterostrophus to a plant phenolic, ferulic acid
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ABSTRACT:
PROVIDER: PRJNA515621 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8450650.fastq.gz | Fastqsanger.gz | |||
| SRR8450660.fastq.gz | Fastqsanger.gz | |||
| SRR8450670.fastq.gz | Fastqsanger.gz | |||
| SRR8450651.fastq.gz | Fastqsanger.gz | |||
| SRR8450661.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:The presence of anti-microbial phenolic compounds, such as the model compound ferulic acid, in biomass hydrolysates poses significant challenges to the widespread use of biomass in conjunction with whole cell biocatalysis or fermentation. Currently, these inhibitory compounds must be removed through additional downstream processing to create feedstock suitable for most industrially important microbial strains. This study explores the high ferulic acid tolerance in Lactobacillus brevis (L. brevis), a lactic acid bacteria often found in fermentation processes, by global transcriptional response analysis. The transcriptional profile of L. brevis under ferulic acid stress reveals that the presence of ferulic acid primarily triggers the expression of membrane proteins to counteract ferulic acid induced changes in membrane fluidity and ion leakage, in the midst of a generalized stress response. Several promising routes for understanding phenolic acid tolerance have been identified based upon these findings. These insights may be used to guide further engineering of model industrial organisms to better tolerate phenolic compounds in processed biomass.
2011-12-31 | GSE22826 | GEO
Project description:The presence of anti-microbial phenolic compounds, such as the model compound ferulic acid, in biomass hydrolysates poses significant challenges to the widespread use of biomass in conjunction with whole cell biocatalysis or fermentation. Currently, these inhibitory compounds must be removed through additional downstream processing to create feedstock suitable for most industrially important microbial strains. This study explores the high ferulic acid tolerance in Lactobacillus brevis (L. brevis), a lactic acid bacteria often found in fermentation processes, by global transcriptional response analysis. The transcriptional profile of L. brevis under ferulic acid stress reveals that the presence of ferulic acid primarily triggers the expression of membrane proteins to counteract ferulic acid induced changes in membrane fluidity and ion leakage, in the midst of a generalized stress response. Several promising routes for understanding phenolic acid tolerance have been identified based upon these findings. These insights may be used to guide further engineering of model industrial organisms to better tolerate phenolic compounds in processed biomass. Three biological replicates were utilized for each time point. Total RNA was extracted using the Zymo Research Bacterial/Fungal RNA extraction kit Microarrays were indirectly labeled, hybridized, and washed according to the Fairplay III Kit protocol. Slides were scanned using the Axon GenePix 4200A scanner. Data normalization (LOWESS) was carried out on each array separately. The arithmetic average of probe signals was used to compute Log2 values.
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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.
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