Nitric oxide mediates the fungal elicitor-induced puerarin biosynthesis in Pueraria thomsonii Benth. suspension cells through a salicylic acid (SA)-dependent and a jasmonic acid (JA)-dependent signal pathway
Nitric oxide mediates the fungal elicitor-induced puerarin biosynthesis in Pueraria thomsonii Benth. suspension cells through a salicylic acid (SA)-dependent and a jasmonic acid (JA)-dependent signal pathway
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DOI：
10.1007/s11427-006-2010-5
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发表时间：
2006-08
期刊：
影响因子：
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通讯作者：
Maojun Xu;Jufang Dong;Mu-yuan Zhu
中科院分区：
文献类型：
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作者：
Maojun Xu;Jufang Dong;Mu-yuan Zhu
一氧化氮（NO）是近年来发现的植物次生代谢产物合成的重要信号分子。为了探讨NO信号在激发子诱导植物细胞次生代谢产物合成中的分子基础，测定了葛根中NO、水杨酸（SA）、茉莉酸（JA）和葛根素的含量。用从桔青霉细胞壁制备的激发子处理悬浮细胞。结果表明，真菌诱导子诱导了P.汤姆森细胞一氧化氮特异性清除剂cPITO可抑制激发子诱导的SA积累和葛根素的合成，表明NO是激发子诱导的SA和葛根素合成所必需的。汤姆森细胞在转基因NahGP中。汤姆森细胞，真菌诱导子也诱导葛根素的生物合成，NO爆发，和JA的积累，虽然SA的生物合成受损。cPITO可阻断激发子诱导的JA在转基因细胞中的积累，表明JA作用于NO的下游，其生物合成受NO控制。外源NO通过其供体硝普钠（SNP）促进转基因NahGP中葛根素的生物合成。汤姆森JA抑制剂IBU和NDGA可抑制NO诱导的葛根素合成，表明NO通过JA依赖的信号途径诱导转基因细胞中葛根素的合成。外源SA抑制了激发子诱导的JA生物合成，并逆转了IBU和NDGA对激发子诱导的葛根素合成的抑制作用，表明SA抑制了细胞内JA的生物合成，SA可能作为JA的替代物参与了激发子和NO诱导的葛根素合成。因此，NO可能通过SA和JA依赖的信号通路介导野生型P.汤姆森细胞和转基因NahG细胞。
Nitric oxide (NO) has emerged as a key signaling molecule in plant secondary metabolite biosynthesis recently. In order to investigate the molecular basis of NO signaling in elicitor-induced secondary metabolite biosynthesis of plant cells, we determined the contents of NO, salicylic acid (SA), jasmonic acid (JA), and puerarin inPueraria thomsoniiBenth. suspension cells treated with the elicitors prepared from cell walls ofPenicillium citrinum. The results showed that the fungal elicitor induced NO burst, SA accumulation and puerarin production ofP. thomsoniiBenth. cells. The elicitor-induced SA accumulation and puerarin production was suppressed by nitric oxide specific scavenger cPITO, indicating that NO was essential for elicitor-induced SA and puerarin biosynthesis inP. thomsoniiBenth. cells. In transgenic NahGP. thomsoniiBenth. cells, the fungal elicitor also induced puerarin biosynthesis, NO burst, and JA accumulation, though the SA biosynthesis was impaired. The elicitor-induced JA accumulation in transgenic cells was blocked by cPITO, which suggested that JA acted downstream of NO and its biosynthesis was controlled by NO. External application of NO via its donor sodium nitroprusside (SNP) enhanced puerarin biosynthesis in transgenic NahGP. thomsoniiBenth. cells, and the NO-triggered puerarin biosynthesis was suppressed by JA inhibitors IBU and NDGA, which indicated that NO induced puerarin production through a JA-dependent signal pathway in the transgenic cells. Exogenous application of SA suppressed the elicitor-induced JA biosynthesis and reversed the inhibition of IBU and NDGA on elicitor-induced puerarin accumulation in transgenic cells, which indicated that SA inhibited JA biosynthesis in the cells and that SA might be used as a substitute for JA to mediate the elicitor-and NO-induced puerarin biosynthesis. It was, therefore, concluded that NO might mediate the elicitor-induced puerarin biosynthesis through SA-and JA-dependent signal pathways in wildtypeP. thomsoniiBenth. cells and transgenic NahG cells respectively.