Instituto de Biología Molecular y Celular de Plantas (IBMCP), Universidad Politécnica de Valencia (UPV)-Consejo Superior de Investigaciones Científicas (CSIC), Ciudad Politécnica de la Innovación (CPI), Valencia, Spain.
PLoS One. 2013;8(1):e55115. doi: 10.1371/journal.pone.0055115. Epub 2013 Jan 30.
Resistance to biotrophic pathogens is largely dependent on the hormone salicylic acid (SA) while jasmonic acid (JA) regulates resistance against necrotrophs. JA negatively regulates SA and is, in itself, negatively regulated by SA. A key component of the JA signal transduction pathway is its receptor, the COI1 gene. Mutations in this gene can affect all the JA phenotypes, whereas mutations in other genes, either in JA signal transduction or in JA biosynthesis, lack this general effect. To identify components of the part of the resistance against biotrophs independent of SA, a mutagenised population of NahG plants (severely depleted of SA) was screened for suppression of susceptibility. The screen resulted in the identification of intragenic and extragenic suppressors, and the results presented here correspond to the characterization of one extragenic suppressor, coi1-40. coi1-40 is quite different from previously described coi1 alleles, and it represents a strategy for enhancing resistance to biotrophs with low levels of SA, likely suppressing NahG by increasing the perception to the remaining SA. The phenotypes of coi1-40 lead us to speculate about a modular function for COI1, since we have recovered a mutation in COI1 which has a number of JA-related phenotypes reduced while others are equal to or above wild type levels.
对生物寄生病原体的抗性在很大程度上依赖于激素水杨酸（SA），而茉莉酸（JA）则调节对坏死病原体的抗性。JA 负调节 SA，本身也受 SA 负调节。JA 信号转导途径的一个关键组成部分是其受体 COI1 基因。该基因的突变会影响所有的 JA 表型，而其他基因（无论是在 JA 信号转导还是在 JA 生物合成中）的突变则缺乏这种普遍效应。为了鉴定与 SA 无关的生物寄生抗性部分的组成部分，对严重缺乏 SA 的 NahG 植株的诱变群体进行了筛选，以寻找对敏感性的抑制作用。筛选结果鉴定出了基因内和基因外的抑制子，这里呈现的结果对应于一个基因外抑制子 coi1-40 的特征。 coi1-40 与先前描述的 coi1 等位基因非常不同，它代表了一种用低水平 SA 增强对生物寄生抗性的策略，可能通过增加对剩余 SA 的感知来抑制 NahG。 coi1-40 的表型使我们推测 COI1 具有模块化功能，因为我们已经恢复了一个 COI1 突变，该突变的许多与 JA 相关的表型降低，而其他表型则与野生型水平相等或更高。
