Manzo Daniele, Ferriello Francesca, Puopolo Gerardo, Zoina Astolfo, D'Esposito Daniela, Tardella Luca, Ferrarini Alberto, Ercolano Maria Raffaella
Department of Agriculture Sciences, University of Naples 'Federico II', Via Università, 100, 80055, Portici, Italy.
Current address: Sustainable Agro-Ecosystems and Bioresources Department - IASMA Research and Innovation Center - Fondazione Edmund Mach, S. Michele all'Adige, Trento, Italy.
BMC Plant Biol. 2016 Feb 27;16:53. doi: 10.1186/s12870-016-0740-5.
Fusarium oxysporum f.sp. radicis-lycopersici (FORL) is one of the most destructive necrotrophic pathogens affecting tomato crops, causing considerable field and greenhouse yield losses. Despite such major economic impact, little is known about the molecular mechanisms regulating Fusarium oxysporum f.sp. radicis-lycopersici resistance in tomato.
A transcriptomic experiment was carried out in order to investigate the main mechanisms of FORL response in resistant and susceptible isogenic tomato lines. Microarray analysis at 15 DPI (days post inoculum) revealed a distinct gene expression pattern between the two genotypes in the inoculated vs non-inoculated conditions. A model of plant response both for compatible and incompatible reactions was proposed. In particular, in the incompatible interaction an activation of defense genes related to secondary metabolite production and tryptophan metabolism was observed. Moreover, maintenance of the cell osmotic potential after the FORL challenging was mediated by a dehydration-induced protein. As for the compatible interaction, activation of an oxidative burst mediated by peroxidases and a cytochrome monooxygenase induced cell degeneration and necrosis.
Our work allowed comprehensive understanding of the molecular basis of the tomato-FORL interaction. The result obtained emphasizes a different transcriptional reaction between the resistant and the susceptible genotype to the FORL challenge. Our findings could lead to the improvement in disease control strategies.
番茄根腐尖孢镰刀菌（FORL）是影响番茄作物的最具破坏性的坏死营养型病原体之一，会导致田间和温室产量大幅损失。尽管造成了如此重大的经济影响，但对于调控番茄对番茄根腐尖孢镰刀菌抗性的分子机制却知之甚少。
进行了一项转录组学实验，以研究抗性和感病同基因番茄品系对FORL反应的主要机制。接种后15天（dpi）的微阵列分析揭示了在接种与未接种条件下两种基因型之间不同的基因表达模式。提出了植物对亲和与非亲和反应的响应模型。具体而言，在非亲和互作中，观察到与次生代谢产物产生和色氨酸代谢相关的防御基因被激活。此外，FORL侵染后细胞渗透势的维持由一种脱水诱导蛋白介导。至于亲和互作，过氧化物酶和细胞色素单加氧酶介导的氧化爆发激活导致细胞变性和坏死。
我们的工作使人们能够全面了解番茄与FORL互作的分子基础。获得的结果强调了抗性和感病基因型对FORL侵染的不同转录反应。我们的发现可能会带来病害控制策略的改进。
