Project description:Sudden death syndrome (SDS) is caused by the ascomycete fungus, Fusarium virguliforme. The pathogen secretes one or more toxins into the infected soybean roots to cause foliar SDS. This study investigated if the xylem sap of F. virguliforme-infected soybean plants contains secreted F. virguliforme-proteins, some of which could be involved in foliar SDS development.
Project description:Many of the microorganisms that are normally present in the soil, actually inhabit the rhizosphere and interact with plants. Those plant–microorganisms interactions may be beneficial or harmful. Among the first are the arbuscular mycorrhizal fungi (AMF). These soil fungi have been reported to improve plant resistance/tolerance to pests and diseases. On the other hand, soilborne pathogens represent a threat to agriculture generating important yield losses, depending upon the pathogen and the crop. One example is the “Sudden Death Syndrome” (SDS), a severe disease in soybean (Glycine max (L.) Merr) caused by a complex of at least four species of Fusarium sp., among which Fusarium virguliforme and F. tuccumaniae are the most prevalent in Argentina. This study provides, under strict in vitro culture conditions, a global analysis of transcript modifications in mycorrhizal and non-mycorrhizal soybean root associated with F. virguliforme inoculation. Microarray results showed qualitative and quantitative changes in the expression of defense-related genes in mycorrhizal soybean, suggesting that AMF are good candidates for sustainable plant protection against F. virguliforme.
Project description:Microarray experiments allow the dissection genome wide patterns of mRNA abundances and improve understanding of the molecular basis of the plant defense responses. These global and simultaneous analyses of TA profiles enable variations in mRNA abundances under specific treatments to be compared. In order to compare the plant resistance mechanism to DON toxicity and infection of Fusarial pathogens, microarray data from Arabidopsis thaliana cells challenged with the mycotoxin DON was compared to the data from the plants responding to F. virguliforme infestations. The microarray chip contained over 10,000 different ESTs (AFGC) was employed in both analyses. The first objective of this approach was to identify genes that were transcriptionally regulated when plants were treated with the toxin. The second objective using the microarray data was to identify resistance pathways where these co-regulated genes were positioned. The parallel comparison on transcriptional activities among soybean and Arabidopsis after fungal pathogen Fsg pathogenesis and Arabidopsis with DON treatment was also performed. Infection: Using F. virguliforme spores Compound Based Treatment: Time seedlings were exposed to Deoxynivalenol time_series_design
Project description:Microarray experiments allow the dissection genome wide patterns of mRNA abundances and improve understanding of the molecular basis of the plant defense responses. These global and simultaneous analyses of TA profiles enable variations in mRNA abundances under specific treatments to be compared. In order to compare the plant resistance mechanism to DON toxicity and infection of Fusarial pathogens, microarray data from Arabidopsis thaliana cells challenged with the mycotoxin DON was compared to the data from the plants responding to F. virguliforme infestations. The microarray chip contained over 10,000 different ESTs (AFGC) was employed in both analyses. The first objective of this approach was to identify genes that were transcriptionally regulated when plants were treated with the toxin. The second objective using the microarray data was to identify resistance pathways where these co-regulated genes were positioned. The parallel comparison on transcriptional activities among soybean and Arabidopsis after fungal pathogen Fsg pathogenesis and Arabidopsis with DON treatment was also performed. Infection: Using F. virguliforme spores Compound Based Treatment: Time seedlings were exposed to Deoxynivalenol
