中文摘要：

从大丽轮枝菌（Verticillium dahliae）的胞外分泌物中分离到一种蛋白激发子PevD1（UniProtKBaccession No.P86840）。为了明确该蛋白激发子的特性以及诱导植物抗病的机制,本研究在大肠杆菌（Escherichia coli）中表达了重组蛋白6His-PevD1。该重组蛋白激发子可以引起烟草（Nicotiana tabacumcv.Samsun-NN）悬浮细胞死亡,提高烟草植株对烟草花叶病毒（TMV）的系统获得抗性（SAR）,枯斑抑制率最高可达46.64%。重组蛋白激发子处理后的烟草叶片中的苯丙氨酸解氨酶（PAL）、多酚氧化酶（PPO）和过氧化物酶（POD）活性均有大幅度提高。处理后144hPAL活性最大,是对照的3.3倍;处理后120h,PPO和POD活性分别增加236.8%和204.6%。PevD1可以诱导抗性相关基因酸性病程相关基因1（acid pathogenesis-related gene1,PR1-a）、碱性病程相关基因1（basic pathogenesis-related gene1,PR1-b）、病程相关基因非表达子1（nonexpressor of pathogenesis-related gene1,NPR1）和苯丙氨酸解氨酶基因（phenylalanine ammonia lyase gene,PAL）的表达。研究表明,防御相关酶的活性提高和抗病相关基因的诱导表达是PevD1诱导烟草产生系统性抗性的主要机制。

英文摘要：

Protein elicitor from Verticillium dahliae（PevD1,UniProtKB accession No.P86840） was isolated from V.dahliae culture filtrate.To functionally investigate the mechanisms of disease resistance induced by the elicitor,we have expressed and purified the recombinant protein,6His-PevD1 in Escherichia coli,The recombinant protein could cause cell death in tobacco（Nicotiana tabacum cv.Samsun-NN） cell suspension and enhanced the systemic resistance of tobacco to Tobacco mosaic virus（TMV）.The rate of necrosis reduction by the elicitor treatment could be up to 46.64%.The activities of phenylalanine ammonia lyase（PAL）,polyphenol oxidase（PPO） and peroxidase（POD） were increased significantly upon PevD1 treatment in tobacco leaves.The maximal activity of PAL appeared at 144 h post the treatment,which was 3.3 times as high as that of the untreated control.And the activities of PPO and POD increased by 236.8% and 204.6% after 120 h post the treatment,respectively.Transcription of acid pathogenesis-related gene 1（PR1-a）,basic pathogenesis-related gene 1（PR1-b）,non-expresser of pathogenesis-related gene 1（NPR1） and phenylalanine ammonia lyase gene（PAL） was upregulated after PevD1 treatment as well.Taken together,these results demonstrate that the activity enhancement of defense-related enzymes and the induction of resistance-related genes＇ expression are the key mechanisms underlying the systemic acquired resistance（SAR） induced by PevD1 in tobacco.