The involvement of jasmonates and ethylene in Alternaria alternata f. sp. lycopersici toxin-induced tomato cell death

• Published in: Journal of experimental botany 2011-11, Vol.62 (15), p.5405-5418
• Main Authors: Zhang, Liping, Jia, Chengguo, Liu, Lihong, Zhang, Zhiming, Li, Chuanyou, Wang, Qiaomei
• Format: Article
• Language: English
• Subjects: Alternaria; Alternaria alternata; Biological and medical sciences; Biosynthesis; Cell death; Cyclopentanes - metabolism; Ethylenes - metabolism; Fundamental and applied biological sciences. Psychology; Gene expression; Gene Expression Regulation, Plant - drug effects; Genes; Jails; Lycopersicon esculentum; Lycopersicon esculentum - cytology; Lycopersicon esculentum - drug effects; Lycopersicon esculentum - metabolism; Oxylipins - metabolism; Pathogens; Phytopathology. Animal pests. Plant and forest protection; Plant cells; Plant physiology and development; Plants; RESEARCH PAPER; Research Papers; Solanum; Sphingosine - metabolism; Toxins
• ISSN: 0022-0957; 1460-2431
• DOI: 10.1093/jxb/err217

Previous studies have shown that an ethylene (ET)-dependent pathway is involved in the cell death signalling triggered by Alternaria alternata f. sp. lycopersici (AAL) toxin in detached tomato (Solanum lycopersicum) leaves. In this study, the role of jasmonic acid (JA) signalling in programmed cell death (PCD) induced by AAL toxin was analysed using a 35S::prosystemin transgenic line (35S::prosys), a JA-deficient mutant spr2, and a JA-insensitive mutant jai1. The results indicated that JA biosynthesis and signalling play a positive role in the AAL toxin-induced PCD process. In addition, treatment with the exogenous ET action inhibitor silver thiosulphate (STS) greatly suppressed necrotic lesions in 35S::prosys leaves, although 35S::prosys leaflets co-treated with AAL toxin and STS still have a significant high relative conductivity. Application of 1-aminocyclopropane-1-carboxylic acid (ACC) markedly enhanced the sensitivity of spr2 and jai1 mutants to the toxin. However, compared with AAL toxin treatment alone, exogenous application of JA to the ET-insensitive mutant Never ripe (Nr) did not alter AAL toxin-induced cell death. In addition, the reduced ET-mediated gene expression in jai1 leaves was restored by co-treatment with ACC and AAL toxin. Furthermore, JA treatment restored the decreased expression of ET biosynthetic genes but not ET-responsive genes in the Nr mutant compared with the toxin treatment alone. Based on these results, it is proposed that both JA and ET promote the AAL toxin-induced cell death alone, and the JAI receptor-dependent JA pathway also acts upstream of ET biosynthesis in AAL toxin-triggered PCD.