Involvement of cathepsin B in the plant disease resistance hypersensitive response
Involvement of cathepsin B in the plant disease resistance hypersensitive response
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DOI：
10.1111/j.1365-313x.2007.03226.x
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发表时间：
2007-10-01
期刊：
影响因子：
7.2
通讯作者：
Birch, Paul R. J.
中科院分区：
文献类型：
--
作者：
Gilroy, Eleanor M.;Hein, Ingo;Birch, Paul R. J.
多种多样的植物蛋白酶与病原体感知以及随后的抗病信号传导和执行有关。我们利用蛋白酶抑制剂和病毒诱导的基因沉默（VIGS）证明，植物木瓜蛋白酶半胱氨酸蛋白酶组织蛋白酶B是抗病超敏反应（HR）所必需的。组织蛋白酶B的VIGS阻止了两种不同的非宿主细菌病原体诱导的程序性细胞死亡（PCD）和降低了疾病抗性。对马铃薯R3a和疫霉菌Avr3a基因瞬时共表达引发的HR也有抑制作用。然而，在番茄Cf-4对黄枝孢霉AVR4的识别后，组织蛋白酶B的vgs并没有影响到植物的PCD，这表明植物的PCD可以独立于组织蛋白酶B。非宿主对淀粉弧菌的HR伴随着组织蛋白酶B转录水平和酶活性的短暂增加以及HR标记基因Hsr203的诱导。组织蛋白酶B的vgs显著降低了E. amylovora攻击后Hsr203的诱导，进一步证明了该蛋白酶在PCD中的作用。在动物PCD过程中，组织蛋白酶B通常从溶酶体重新定位到细胞质中，而植物组织蛋白酶B则分泌到外质体中，并在没有病原体攻击的情况下被激活。
A diverse range of plant proteases are implicated in pathogen perception and in subsequent signalling and execution of disease resistance. We demonstrate, using protease inhibitors and virus-induced gene silencing (VIGS), that the plant papain cysteine protease cathepsin B is required for the disease resistance hypersensitive response (HR). VIGS of cathepsin B prevented programmed cell death (PCD) and compromised disease resistance induced by two distinct non-host bacterial pathogens. It also suppressed the HR triggered by transient co-expression of potato R3a and Phytophthora infestans Avr3a genes. However, VIGS of cathepsin B did not compromise HR following recognition of Cladosporium fulvum AVR4 by tomato Cf-4, indicating that plant PCD can be independent of cathepsin B. The non-host HR to Erwinia amylovora was accompanied by a transient increase in cathepsin B transcript level and enzymatic activity and induction of the HR marker gene Hsr203. VIGS of cathepsin B significantly reduced the induction of Hsr203 following E. amylovora challenge, further demonstrating a role for this protease in PCD. Whereas cathepsin B is often relocalized from the lysosome to the cytosol during animal PCD, plant cathepsin B is secreted into the apoplast, and is activated upon secretion in the absence of pathogen challenge.