Hu Xiangyang, Neill Steven J, Cai Weiming, Tang Zhangcheng
Shanghai Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Shanghai,200032, China.
Centre for Research in Plant Science, University of the West of England, Coldharbour Lane, Bristol,FrenchayBS16 1QY, UK.
Funct Plant Biol. 2003 Sep;30(8):901-907. doi: 10.1071/FP03061.
The elicitor oligogalacturonic acid (OGA) stimulated nitric oxide (NO) accumulation in the growth medium of ginseng suspension cultures and induced increased nitric oxide synthase (NOS) activity in ginseng cells. OGA also stimulated accumulation of saponin, transcription of genes encoding squalene synthase (sqs) and squalene epoxidase (sqe), two early enzymes of saponin synthesis, and the accumulation of β-amyrin synthase protein (β-AS). Saponin accumulation, sqs and sqe gene expression, and increases in β-AS content were also induced by exposure to NO via the NO donor sodium nitroprusside (SNP). Inhibitors of mammalian nitric oxide synthase reduced both OGA-induced NO accumulation and NOS activity, suggesting that OGA-induced NO production occurs via a NOS-like enzyme. OGA-induced accumulation of β-AS and saponin, and transcription of sqs and sqe, were suppressed by treatments that removed NO or inhibited its production, indicating a role for NO in mediating OGA effects on these defence responses. NO accumulation and increased NOS activity were inhibited by calcium channel inhibitors and a protein kinase inhibitor, but not by a protein phosphatase inhibitor, indicating the requirement for calcium and protein phosphorylation during OGA-induced NO production. Saponin production and transcription, and accumulation of saponin biosynthetic genes and enzymes were also suppressed by these treatments, as well as by the protein phosphatase inhibitor okadaic acid.
激发子寡聚半乳糖醛酸（OGA）刺激人参悬浮培养物生长培养基中一氧化氮（NO）的积累，并诱导人参细胞中一氧化氮合酶（NOS）活性增加。OGA还刺激了人参皂苷的积累、编码鲨烯合酶（sqs）和鲨烯环氧酶（sqe）（皂苷合成的两种早期酶）的基因转录以及β-香树素合酶蛋白（β-AS）的积累。通过NO供体硝普钠（SNP）暴露于NO也可诱导人参皂苷的积累、sqs和sqe基因表达以及β-AS含量的增加。哺乳动物一氧化氮合酶抑制剂可降低OGA诱导的NO积累和NOS活性，这表明OGA诱导的NO产生是通过一种类NOS酶发生的。去除NO或抑制其产生的处理可抑制OGA诱导的β-AS和人参皂苷的积累以及sqs和sqe的转录，这表明NO在介导OGA对这些防御反应的影响中发挥作用。钙通道抑制剂和蛋白激酶抑制剂可抑制NO积累和NOS活性增加，但蛋白磷酸酶抑制剂则无此作用，这表明在OGA诱导的NO产生过程中需要钙和蛋白磷酸化。这些处理以及蛋白磷酸酶抑制剂冈田酸也可抑制人参皂苷的产生和转录以及人参皂苷生物合成基因和酶的积累。
