Abstract
Abstract Phytophthora infestans, the cause of potato and tomato late blight disease, produces INF1 elicitin, a 10 kDa extracellular protein. INF1 induces a hypersensitive response (HR) and systemic acquired resistance in species of the Nicotiana genus and a few other genera. We analysed the response of tomato to INF1 and INF1S3, which has a Cys to Ser substitution at position 3 of the processed protein and therefore lacks HR induction activity in tobacco. No HR cell death was induced in either INF1‐ or INF1S3‐treated tomato leaves. The expression of salicylic acid (SA)‐responsive PR‐1a(P6) and PR‐2a genes was not induced by treatment with either INF1 or INF1S3. However, the expression of jasmonic acid (JA)‐responsive PR‐6 encoding proteinase inhibitor II, LeATL6 encoding ubiquitin ligase E3, and LOX‐E encoding lipoxygenase, was up‐regulated in tomato leaves treated with INF1 but not in those treated with INF1S3. Their induction was completely compromised in INF1‐treated jai1‐1 mutant tomato, in which the JA signalling pathway is impaired. The accumulation of ethylene (ET) and the expression of ET‐responsive genes were also induced in tomato by INF1 but not INF1S3 treatment. The activation of JA and ET‐mediated signals but not the SA‐mediated signalling in INF1‐treated tomato was also demonstrated by global gene expression analysis. INF1‐treated tomatoes, but not those treated with INF1S3, exhibited resistance to bacterial wilt disease caused by Ralstonia solanacearum. Thus, INF1 seems to induce resistance to bacterial wilt disease in tomato and activate JA‐ and ET‐mediated signalling pathways without development of HR cell death.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.