4.7 Article

Rapid induction of a protein disulfide isomerase and defense-related genes in wheat in response to the hemibiotrophic fungal pathogen Mycosphaerella graminicola

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PLANT MOLECULAR BIOLOGY
卷 53, 期 5, 页码 741-754

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SPRINGER
DOI: 10.1023/B:PLAN.0000019120.74610.52

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defense response; differential-display PCR; Mycosphaerella graminicola; protein disulfide isomerase; Septoria tritici blotch; real-time quantitative RT-PCR

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Mycosphaerella graminicola, incitant of septoria tritici blotch, is a widespread and significant pathogen of wheat that is not closely related to other fungi being developed as genetic models for host-pathogen interactions. Several resistance genes in wheat have been identified, yet the molecular mechanisms of resistance are unknown. To identify host genes involved in the resistance response, expression profiles of the wheat line Tadinia (containing the Stb4 gene for resistance) and the susceptible line Yecora Rojo, non-inoculated or inoculated with M. graminicola, were compared by differential-display polymerase chain reaction (DD-PCR). Among the differentially expressed genes was a protein disulfide isomerase (PDI), which is well known as a molecular chaperone and component of signal-transduction pathways in animal systems but had not been implicated previously in plant defense response. Real-time quantitative reverse-transcription PCR and northern analysis revealed that PDI was induced within 3 h of inoculation with highest induction in the pathogen-treated resistant lines. These responses of PDI were similar to the early and strong resistance-related responses displayed by the pathogenesis-related (PR) proteins, PR-1, PR-2 and PR-5. In contrast, a wheat lipoxygenase was down-regulated in the resistant lines at time points corresponding with peak induction of the PR genes. Thus, part of the resistance mechanism may involve repression of a gene that could otherwise aid fungal growth. Wheat responds much more rapidly than believed previously to signals produced by M. graminicola. These early responses begin prior to penetration of the host and appear to determine the outcome of the host-pathogen interaction.

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