一氧化氮合酶途径在精氨酸诱导番茄果实采后抗病性中的作用

以绿熟期‘中蔬4号’番茄果实为实验材料,研究了精氨酸(arginine,Arg)对番茄果实灰霉病发生的影响及一氧化氮合酶(nitric oxide synthase,NOS)途径在其中的作用及机制。结果表明:0.0~10.0 mmol/L范围内,5.0 mmol/L的Arg对番茄果实灰霉病的发生率及病斑面积的扩展控制效果最佳。同时5.0 mmol/L Arg处理明显提高了番茄果实NOS活力及NO含量,促进了酚类物质的积累,提高了番茄果实体内苯丙氨酸解氨酶、多酚氧化酶、β-1,3-葡聚糖酶和几丁质酶等抗病相关酶的活力,诱导了病程相关蛋白(pathogenesis-related proteins,PRs)PR2a、PR2b、PR3a和PR3b的表达。而NOS抑制剂N-硝基-L-精氨酸通过抑制NOS的活力和NO的水平,明显削弱了Arg对番茄果实的这种诱导作用,因此Arg可能是通过调控NOS途径诱导了番茄果实抵抗灰霉病的抗性。

Role of Nitric Oxide Synthase Pathway in Arginine-Induced Disease Resistance in Postharvest Tomato Fruit

This study aimed to investigate the effect of arginine treatment on the occurrence of postharvest gray mold in ‘Zhongshu No. 4’ tomato fruit and the role and mechanism of nitric oxide synthase (NOS) pathway in arginine-induced disease resistance during storage at (25 ± 1) ℃. The results indicated that 5.0 mmol/L arginine was the most effective treatment in reducing the incidence of gray mold and lesion area in tomato fruit in the concentration range of 0.0–10.0 mmol/L. Moreover, 5.0 mmol/L arginine treatment increased NOS activity and nitric oxide (NO) content. Total phenol content and the activities of phenylalanine ammonia-lyase, polyphenol oxidase, chitinase and β-1,3-glucanase were also enhanced remarkably. Besides, the expression of pathogenesis-related genes (PR2a, PR2b, PR3a and PR3b) were induced significantly. However, these effects were partially counteracted by Nω-nitro-L-arginine, an inhibitor of NOS. Our results indicate that arginine-induced resistance to gray mold in postharvest tomato fruit may be due to promoting the NOS pathway.