BACKGROUND Plants are exposed to various forms of environmental stress. Penetration by pathogens is one of the most serious environmental insults. Wounding caused by tissue damage or herbivory also affects the growth and reproduction of plants. Moreover, wounding disrupts physical barriers present at the plant surface and increases the risk of pathogen invasion. Plants cope with environmental stress by inducing a variety of responses. These stress responses must be tightly controlled, because their unnecessary induction is detrimental to plant growth. In tobacco, WIPK and SIPK, two wound-responsive mitogen-activated protein kinases, have been shown to play important roles in regulating wound responses. However, their contribution to downstream wound responses such as gene expression is not well understood. RESULTS To identify genes regulated by WIPK and SIPK, the transcriptome of wounded WIPK/SIPK-suppressed plants was analyzed. Among the genes down-regulated in WIPK/SIPK-suppressed plants, the largest group consisted of those involved in the production of antimicrobial phytoalexins. Almost all genes involved in the biosynthesis of capsidiol, a major phytoalexin in tobacco, were transcriptionally induced by wounding in WIPK/SIPK-dependent and -independent manners. 5-epi-aristolochene synthase (EAS) is the committing enzyme for capsidiol synthesis, and the promoter of EAS4, a member of the EAS family, was analyzed. Reporter gene analysis revealed that at least two regions each 40-50 bp length were involved in activation of the EAS4 promoter by wounding, as well as by artificial activation of WIPK and SIPK. Unlike transcripts of the capsidiol synthesis genes, accumulation of EAS protein and capsidiol itself were not induced by wounding; however, wounding significantly enhanced their subsequent induction by a pathogen-derived elicitor. CONCLUSIONS Our results suggest a so-called priming phenomenon since the induction of EAS by wounding is only visible at the transcript level. By inducing transcripts, not the proteins, of EAS and possibly other capsidiol synthesis genes at wound sites, plants can produce large quantities of capsidiol quickly if pathogens invade the wound site, whereas plants can minimize energy loss and avoid the cytotoxic effects of capsidiol where pathogens do not gain entry during wound healing.

中文翻译：

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通过损伤来转录诱导辣椒素合成基因可以促进病原体信号诱导的辣椒素合成。


背景技术植物暴露于各种形式的环境胁迫。病原体的渗透是最严重的环境侵害之一。组织损伤或食草造成的伤害也会影响植物的生长和繁殖。此外，受伤会破坏植物表面的物理屏障，增加病原体入侵的风险。植物通过诱导多种反应来应对环境压力。必须严格控制这些胁迫反应，因为不必要的诱导对植物生长有害。在烟草中，WIPK 和 SIPK 这两种伤口反应性丝裂原激活蛋白激酶已被证明在调节伤口反应中发挥重要作用。然而，它们对下游伤口反应（例如基因表达）的贡献尚不清楚。结果 为了鉴定受 WIPK 和 SIPK 调节的基因，对受伤的 WIPK/SIPK 抑制植物的转录组进行了分析。在 WIPK/SIPK 抑制的植物中下调的基因中，最大的一组是那些参与抗菌植物抗毒素生产的基因。几乎所有参与辣椒素生物合成的基因（烟草中的一种主要植物抗毒素）都是通过损伤以 WIPK/SIPK 依赖性和非依赖性方式转录诱导的。 5-表-马兜铃烯合酶(EAS)是Capsidiol合成的关键酶，对EAS家族成员EAS4的启动子进行了分析。报告基因分析显示，至少有两个长度各为 40-50 bp 的区域参与了 EAS4 启动子通过损伤以及人工激活 WIPK 和 SIPK 的激活。 与辣椒素合成基因的转录物不同，EAS蛋白和辣椒素本身的积累不是由受伤引起的；然而，受伤显着增强了病原体衍生的激发子对它们的后续诱导。结论 我们的结果表明存在所谓的启动现象，因为受伤引起的 EAS 仅在转录水平可见。通过在伤口部位诱导 EAS 和可能的其他辣椒素合成基因的转录本，而不是蛋白质，如果病原体侵入伤口部位，植物可以快速产生大量辣椒素，而当病原体入侵伤口时，植物可以最大限度地减少能量损失并避免辣椒素的细胞毒性作用。伤口愈合期间请勿进入。