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本氏烟草对致病疫霉的抗性是由激发子蛋白INF1的识别介导的。

Resistance of nicotiana benthamiana to phytophthora infestans is mediated by the recognition of the elicitor protein INF1.

作者信息

Kamoun S, Vleeshouwers VG, Govers F

机构信息

Laboratory of Phytopathology and Graduate School, Experimental Plant Sciences, Wageningen Agricultural University, Wageningen, The Netherlands.

出版信息

Plant Cell. 1998 Sep;10(9):1413-26. doi: 10.1105/tpc.10.9.1413.

Abstract

Phytophthora infestans, the agent of potato and tomato late blight disease, produces a 10-kD extracellular protein, INF1 elicitin. INF1 induces a hypersensitive response in a restricted number of plants, particularly those of the genus Nicotiana. In virulence assays with different P. infestans isolates, five Nicotiana species displayed resistance responses. In all of the interactions, after inoculation with P. infestans zoospores, penetration of an epidermal cell was observed, followed by localized necrosis typical of a hypersensitive response. To determine whether INF1 functions as an avirulence factor in these interactions, we adopted a gene-silencing strategy to inhibit INF1 production. Several transformants deficient in inf1 mRNA and INF1 protein were obtained. These strains remained pathogenic on host plants. However, in contrast to the wild-type and control transformant strains, INF1-deficient strains induced disease lesions when inoculated on N. benthamiana. These results demonstrate that the elicitin INF1 functions as an avirulence factor in the interaction between N. benthamiana and P. infestans.

摘要

致病疫霉是马铃薯和番茄晚疫病的病原体,它能产生一种10千道尔顿的细胞外蛋白——激发素INF1。INF1能在有限数量的植物中诱导过敏反应,尤其是烟草属植物。在对不同致病疫霉分离株的毒力测定中,有五种烟草属植物表现出抗性反应。在所有这些相互作用中,接种致病疫霉游动孢子后,观察到其穿透表皮细胞,随后出现典型过敏反应的局部坏死。为了确定INF1在这些相互作用中是否作为无毒因子起作用,我们采用基因沉默策略来抑制INF1的产生。获得了几个缺乏inf1 mRNA和INF1蛋白的转化体。这些菌株在寄主植物上仍具致病性。然而,与野生型和对照转化体菌株不同,缺乏INF1的菌株接种到本氏烟草上时会诱导病害病斑。这些结果表明,激发素INF1在本氏烟草与致病疫霉的相互作用中作为无毒因子起作用。

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