Key Laboratory of Horticultural Plant Growth, Development and Quality Improvement, Ministry of Agriculture, Department of Horticulture, Zhejiang University, Hangzhou 310058, China.
J Exp Bot. 2011 Nov;62(15):5405-18. doi: 10.1093/jxb/err217. Epub 2011 Aug 23.
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 JAI1 receptor-dependent JA pathway also acts upstream of ET biosynthesis in AAL toxin-triggered PCD.
先前的研究表明，乙烯（ET）依赖性途径参与了由Alternaria alternata f. sp. lycopersici（AAL）毒素在离体番茄（Solanum lycopersicum）叶片中引发的细胞死亡信号转导。在这项研究中，使用 35S::prosystemin 转基因系（35S::prosys）、茉莉酸（JA）缺陷突变体 spr2 和 JA 不敏感突变体 jai1 分析了 JA 信号在 AAL 毒素诱导的程序性细胞死亡（PCD）中的作用。结果表明，JA 的生物合成和信号转导在 AAL 毒素诱导的 PCD 过程中发挥了积极作用。此外，用外源 ET 作用抑制剂硫代硫酸银（STS）处理极大地抑制了 35S::prosys 叶片的坏死损伤，尽管 AAL 毒素和 STS 共处理的 35S::prosys 小叶仍具有显著高的相对电导率。1-氨基环丙烷-1-羧酸（ACC）的应用显著增强了 spr2 和 jai1 突变体对毒素的敏感性。然而，与 AAL 毒素单独处理相比，外源 JA 对 ET 不敏感突变体 Never ripe（Nr）的应用并未改变 AAL 毒素诱导的细胞死亡。此外，ACC 和 AAL 毒素共处理恢复了 jai1 叶片中减少的 ET 介导的基因表达。此外，与毒素单独处理相比，JA 处理恢复了 Nr 突变体中 ET 生物合成基因的表达降低，但没有恢复 ET 响应基因的表达。基于这些结果，提出了 JA 和 ET 都单独促进 AAL 毒素诱导的细胞死亡，并且 JAI1 受体依赖性 JA 途径也在 AAL 毒素触发的 PCD 中作为 ET 生物合成的上游作用。
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