Arabidopsis signal transduction mutant defective in chemically and biologically induced disease resistance.

Plants possess multiple resistance mechanisms that guard against pathogen attack. Among these are inducible systems such as systemic acquired resistance (SAR). SAR is activated by pathogen exposure and leads to an increase in salicylic acid (SA), high-level expression of SAR-related genes, and resistance to a spectrum of pathogens. To identify components of the signal transduction pathways regulating SAR, a mutant screen was developed that uses 2,6-dichloroisonicotinic acid as an activator of SAR gene expression and pathogen resistance, followed by assays for resistance to the fungal pathogen Peronospora parasitica. Mutants from this screen were subsequently examined to assess their defense responses. We describe here a recessive mutation that causes a phenotype of insensitivity to chemical and biological inducers of SAR genes and resistance. These data indicate the existence of a common signaling pathway that couples these diverse stimuli to induction of SAR genes and resistance. Because of its non-inducible immunity phenotype, we call this mutant nim1. Although nim1 plants fail to respond to SA, they retain the ability to accumulate wild-type levels of SA, a probable endogenous signal for SAR. Further, the ability of nim1 plants to support growth of normally incompatible races of a fungal pathogen indicates a role for this pathway in expression of genetically determined resistance, consistent with earlier findings for transgenic plants engineered to break down SA. These results suggest that the wild-type NIM1 gene product functions in a pathway regulating acquired resistance, at a position downstream of SA accumulation and upstream of SAR gene induction and expression of resistance. IMAGES:

植物拥有多种抵御病原菌侵染的抗病机制，其中包含诸如系统获得性抗性（systemic acquired resistance, SAR）这类诱导性防御系统。SAR可被病原菌侵染激活，伴随水杨酸（salicylic acid, SA）含量升高、SAR相关基因的高水平表达，以及对广谱病原菌的抗性。为鉴定调控SAR的信号转导通路组分，研究人员开发了一套突变体筛选体系：以2,6-二氯异烟酸（2,6-dichloroisonicotinic acid）作为SAR基因表达与抗病性的诱导剂，随后通过接种真菌病原菌寄生霜霉（Peronospora parasitica）开展抗性检测。后续对该筛选得到的突变体进行了防御响应相关评估。本文报道了一处隐性突变，该突变会使植株对SAR基因与抗病性的化学、生物诱导剂均呈现不敏感表型。上述数据表明存在一条共同的信号通路，可将这些多样的刺激信号耦联至SAR基因的诱导表达与抗病性形成。鉴于该突变体表现为不可诱导免疫表型，我们将其命名为nim1。尽管nim1植株无法响应SA，但它们仍能够积累野生型水平的SA——这是一种潜在的SAR内源信号分子。此外，nim1植株能够支持原本不相容的真菌病原菌生理小种增殖，这表明该信号通路在遗传决定的抗性表达中发挥作用，这与此前通过工程化降解SA的转基因植物得到的研究结果相符。上述结果提示，野生型NIM1基因的编码产物在调控获得性抗性的信号通路中发挥功能，其作用位点位于SA积累的下游，且介于SAR基因诱导与抗病性表达的上游。IMAGES: