Kunitz Trypsin Inhibitor： An Antagonist of Cell Death Triggered by Phytopathogens and Fumonisin B1 in Arabidopsis
Kunitz Trypsin Inhibitor： An Antagonist of Cell Death Triggered by Phytopathogens and Fumonisin B1 in Arabidopsis作者机构：Viikki Biocenter Department of Biological and Environmental Sciences Division of Genetics University of Helsinki POB 56 FIN-00014 Helsinki Finland Current address: Sainsbury Laboratory John Innes Centre Colney Norwich NR4 7UH United Kingdom
出 版 物：《Molecular Plant》 (分子植物（英文版）)
年 卷 期：2008年第1卷第3期
页 面：482-495页
核心收录：
学科分类：0710[理学-生物学] 090603[农学-临床兽医学] 07[理学] 09[农学] 0906[农学-兽医学] 071007[理学-遗传学] 0901[农学-作物学] 0902[农学-园艺学] 090102[农学-作物遗传育种]
主 题：CASPASE-LIKE PROTEASES PATHOGEN ERWINIA-CAROTOVORA HYPERSENSITIVE RESPONSE SERINE-PROTEASE TRANSGENIC PLANTS GENE-EXPRESSION SOYBEAN KUNITZ
摘 要：Programmed cell death （PCD） is a central regulatory process in both plant development and in plant responses to pathogens. PCD requires a coordinate activation of pro-apoptotic factors such as proteases and suppressors inhibiting and modulating these processes. In plants, various caspase-like cysteine proteases as well as serine proteases have been implicated in PCD. Here, we show that a serine protease （Kunitz trypsin） inhibitor （KTI1） of Arabidopsis acts as a functional KTI when produced in bacteria and in planta. Expression of AtKTI1 is induced late in response to bacterial and fungal elicitors and to salicylic acid. RNAi silencing of the AtKTI1 gene results in enhanced lesion development after infiltration of leaf tissue with the PCD-eliciting fungal toxin fumonisin B1 （FB1） or the avirulent bacterial pathogen Pseudomonas syringae pv tomato DC3000 carrying avrB （Pst avrB）. Overexpression of AtKTI1 results in reduced lesion development after Pst avrB and FB1 infiltration. Interestingly, RNAi silencing of AtKTI1 leads to enhanced resistance to the virulent pathogen Erwinia carotovora subsp, carotovora SCC1, while overexpression of AtKTI1 leads to higher susceptibility towards this pathogen. Together, these data indicate that AtKTI1 is involved in modulating PCD in plant-pathogen interactions.
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