Genes and mechanisms in Arabidopsis innate immunity against Leptosphaeria maculans

Leptosphaeria maculans is a hemibiotrophic ascomycete that causes blackleg disease on Brassica oilcrops, which globally is a great threat for oilseed production. In order to obtain mechanistic understanding of this devastating pathogen, Arabidopsis thaliana was used as a model host. Susceptible genotypes of Arabidopsis facilitated identification of the mechanisms required for resistance. The phytoalexin camalexin was first identified as a quantitative resistance factor; whereas accelerated cell death mutants enabled the pathogen to circumvent the resistance mechanisms by switching to a necrotrophic mode of growth. In addition to this, eleven Leptosphaeria maculans susceptible (lms) mutants were identified, one susceptible accession (An-1) and a 1:15 loss of resistance in F2 progenies from the resistant accessions Ler-0 and Col-0. The transgressive segregation revealed that resistance was dependent on TIR-NB-LRR resistance genes (RLM1Col and RLM2Ler), which were independent of signalling components previously associated to all TIR-NB-LRR resistance genes. RLM1Col was found to be responsible for L. maculans induced callose depositions. A segregant analysis of the transcriptomes from resistant and susceptible Col-0 x An-1 F3 lines revealed a region on chromosome 4 with genes significantly more highly expressed in the resistant progenies. T-DNA insertion lines and over expression studies revealed that the N-terminal part of a TIR-NB gene is responsible for resistance to L. maculans, Alternaria brassicae, A. brassicicola and Botrytis cinerea. In contrast to the other pathogens, L. maculans resistance is independent of the phytohormones salicylic acid (SA), jasmonic acid (JA) and ethylene (ET). In order to establish the physiological mechanisms of Arabidopsis L. maculans resistances, characterized mutants defective in other hormone responses were screened. Mutants defective in ABA biosynthesis and signalling were found to impair resistance in both a callose dependent and independent manner. Further analysis of pathogen defence pathways revealed influences from combinations of SA, JA and ET responses on resistance and L. maculans mode of growth when the R gene and camalexin resistances were disrupted. Taken together, this work describes the establishment of a new model pathosystem with well-characterized pathogen and host organisms, which display both novel mechanisms and features overlapping with biotrophic and necrotrophic pathosystems