Chandra S, Martin G B, Low P S
Department of Chemistry, Purdue University, West Lafayette, IN 47907, USA.
Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):13393-7. doi: 10.1073/pnas.93.23.13393.
The Pto gene encodes a serine/threonine kinase that confers resistance in tomato to Pseudomonas syringae pv. tomato strains that express the avirulence gene avrPto. Partial characterization of the Pto signal transduction pathway and the availability of transgenic tomato lines (+/- Pto) make this an ideal system for exploring the molecular basis of disease resistance. In this paper, we test two transgenic tomato cell suspension cultures (+/-Pto) for production of H2O2 following independent challenge with two strains of P. syringae pv. tomato (+/-avrPto). Only when Pto and avrPto are present in the corresponding organisms are two distinct phases of the oxidative burst seen, a rapid first burst followed by a slower and more prolonged second burst. In the remaining three plant-pathogen interactions, we observe either no burst or only a first burst, indicating that the second burst is correlated with disease resistance. Further support for this observation comes from the finding that both resistant and susceptible tomato lines produce the critical second oxidative burst when challenged with P. syringae pv. tabaci, a nonhost pathogen that elicits a hypersensitive response on both tomato lines. The Pto kinase is not required, however, for the oxidative burst initiated by non-specific elicitors such as oligogalacturonides or osmotic stress. A model describing a possible role for the Pto kinase in the overall scheme of oxidative burst signaling is proposed.
Pto基因编码一种丝氨酸/苏氨酸激酶，该激酶使番茄对表达无毒基因avrPto的丁香假单胞菌番茄致病变种菌株产生抗性。对Pto信号转导途径的部分特性分析以及转基因番茄品系（有/无Pto）的可得性，使其成为探索抗病分子基础的理想系统。在本文中，我们用两种丁香假单胞菌番茄致病变种菌株（有/无avrPto）分别对两种转基因番茄细胞悬浮培养物（有/无Pto）进行挑战，检测其H2O2的产生情况。只有当相应生物体中同时存在Pto和avrPto时，才会出现氧化爆发的两个不同阶段，先是快速的第一阶段爆发，接着是较慢且持续时间更长的第二阶段爆发。在其余三种植物 - 病原体相互作用中，我们观察到要么没有爆发，要么只有第一阶段爆发，这表明第二阶段爆发与抗病性相关。对这一观察结果的进一步支持来自以下发现：当用丁香假单胞菌烟草致病变种（一种在两种番茄品系上都引发超敏反应的非寄主病原体）进行挑战时，抗性和感病番茄品系都会产生关键的第二阶段氧化爆发。然而，非特异性激发子（如寡聚半乳糖醛酸苷或渗透胁迫）引发的氧化爆发不需要Pto激酶。本文提出了一个模型，描述了Pto激酶在氧化爆发信号传导总体机制中的可能作用。
