Characterisation of an Arabidopsis–Leptosphaeria maculans pathosystem: resistance partially requires camalexin biosynthesis and is independent of salicylic acid, ethylene and jasmonic acid signalling

• DOI: 10.1046/j.1365-313x.2003.01927.x
• Publication Date: 2003-12-11T17:26:50Z
• Authors: Svante Bohman; Jens Staal; Bart P. H. J. Thomma; Maolin Wang; Christina Dixelius
• Keywords: 0301 basic medicine; Copper Sulfate; Indoles; molecular markers; causal agent; plant defensin gene; Arabidopsis; Cyclopentanes; 03 medical and health sciences; Ascomycota; Plant Growth Regulators; phytoalexin-deficient mutants; Oxylipins; enhanced susceptibility; fragment-length-polymorphism; Plant Diseases; blackleg disease; systemic acquired-resistance; Ethylenes; brassica b-genome; Immunity, Innate; Thiazoles; Mutation; alternaria-brassicicola; Silver Nitrate; Salicylic Acid; Signal Transduction

SummaryOut of 168 Arabidopsis accessions screened with isolates of Leptosphaeria maculans, one (An‐1) showed clear disease symptoms. In order to identify additional components involved in containment of L. maculans in Arabidopsis, a screen for L. maculans‐susceptible (lms) mutants was performed. Eleven lms mutants were isolated, which displayed differential susceptibility responses to L. maculans. lms1 was crossed with Columbia (Col‐0) and Ws‐0, and mapping data for both populations showed the highest linkage to a region on chromosome 2. Reduced levels of PR‐1 and PDF1.2 expression were found in lms1 compared to wild‐type plants 48 h after pathogen inoculation. In contrast, the lms1 mutant displayed upregulation of either marker gene upon chemical treatment, possibly as an effect of an altered ethylene (ET) response. To assess the contribution of different defence pathways, genotypes implicated in salicylic acid (SA) signalling plants expressing the bacterial salicylate hydroxylase (nahG) gene, non‐expressor of PR1 (npr1)‐1 and phytoalexin‐deficient (pad4‐1), jasmonic acid (JA) signalling (coronatine insensitive (coi)1‐16, enhanced disease susceptibility (eds)8‐1 and jasmonic acid resistant (jar)1‐1) and ET signalling (eds4‐1, ethylene insensitive (ein)2, ein3‐1 and ethylene resistant (etr)1‐1) were screened. All the genotypes screened were as resistant as wild‐type plants, demonstrating the dispensability of the pathways in L. maculans resistance. When mutants implicated in cell death responses were assayed, responsive to antagonist 1 (ran1)‐1 exhibited a weak susceptible phenotype, whereas accelerated cell death (acd)1‐20 showed a rapid lesion development. Camalexin is only partially responsible for L. maculans containment in Arabidopsis, as pad3‐1 and enhanced susceptibility to Alternaria (esa)1 clearly showed a susceptible response while wild‐type levels of camalexin were present in An‐1 and lms1. The data presented point to the existence of multiple defence mechanisms controlling the containment of L. maculans in Arabidopsis.