| Summary: | Tomatoes (Solanum lycopersicum ) are produced in all major vegetable growing areas in the world. These plants are exposed to many biotic and abiotic stresses that lead to big losses in yield and high cost of production. The fungus Botrytis cinerea is a major necrotrophic pathogen that preferentially attacks fruits (grapes, strawberries, tomatoes) and flowers, upon which it produces a gray rot. It is also capable of attacking stems, leaves and seeds. Plant immune responses are triggered by pattern recognition receptors that detect pathogen-associated molecular patterns (PAMPs) or by plant disease resistance (R) proteins which recognize matching pathogen avirulence proteins. These recognitions lead to the accumulation of two secondary messengers, salicylic acid (SA) or jasmonic acid (JA), major players in the regulation of signalling networks that are involved in induced defence responses against pathogens. SA acts through the activity of the transcription coactivator NPR1 (nonexpressor of pathogenesis- related (PR) genes), one of the well-known regulators of plant immunity. NPR1 interacts with several TGAs transcription factors which bind to the promoter of the SA-dependent genes including the defence gene PR1 and activates its expression. Some other plant defence responses are controlled by mechanisms dependent on jasmonic acid (JA) that leads to expression of for example defensin gene (PDF1 ) in Arabidopsis thaliana or proteinase inhibitors I and II in tomatoes. SA is required to combat biotrophic pathogens which need live tissues to infect and spread in their hosts; however the JA pathway is essential to destroy necrotrophic pathogens which need dead tissues to cause their disease. SA can antagonise JA and vice versa. The objectives of my thesis were to study whether B. cinerea is able to manipulate the antagonism between SA and JA to cause disease development in tomatoes and the molecular mechanism behind this manipulation if it exists. I have found that B. cinerea manipulates the antagonism between SA and JA to cause its disease development. Indeed, B. cinerea produces an exopolysaccharide called [béta]-(1,3)(1,6)-D-glucan which acts as an inducer of SA. In turn, the SA pathway antagonises the JA signalling pathway, thereby allowing the fungus to develop its disease in tomatoes. Plants compromised in SA accumulation are significantly less susceptible to B. cinerea than the wild type plants. I also showed that the JA-signalling pathway required for tomato resistance against B. cinerea is mediated by the systemin elicitor (The polypeptide systemin is a known elicitor of JA signalling in tomato). I did further studies to dissect the molecular mechanism behind this strategy used by B. cinerea to develop its disease in tomato. I found that NPR1 and TGA1.a are required for disease development caused by this fungus. I also showed that the two JA-dependent defense genes, proteinase inhibitors I and II are important for resistance of tomato against B. cinerea and their expression is negatively regulated by NPR1 and TGA1.a. Finally I have evidence that SA-enhanced susceptibility of tomato to B. cinerea occurs through NPR1 and TGA1.a. Interestingly, I found that Alternaria solani, another necrotrophic pathogen infecting several species including tomatoes uses this strategy to develop its disease in tomato. These data highlight how necrotrophs manipulate SA signalling pathway to promote their disease in the tomato. Thus this study should increase our knowledge in the plant-microbe interaction area.
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