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HSP70s 通过 MAPK 级联增强了疫霉菌效应子诱导的烟草原生质体细胞死亡。

HSP70s Enhance a Phytophthora infestans Effector-Induced Cell Death via an MAPK Cascade in Nicotiana benthamiana.

机构信息

1 Department of Plant Science and Plant Genomics and Breeding Institute, Institute of Agricultural Biotechnology, College of Agriculture and Life Science, Seoul National University, Seoul, 08826, Republic of Korea; and.

2 Institute of Seed Biotechnology, Institute of Green Bio Science and Technology, Seoul National University, Pyeongchang, 25354, Republic of Korea.

出版信息

Mol Plant Microbe Interact. 2018 Mar;31(3):356-362. doi: 10.1094/MPMI-07-17-0156-R. Epub 2018 Jan 25.

DOI:10.1094/MPMI-07-17-0156-R
PMID:29140163
Abstract

A destructive pathogen, Phytophthora infestans, secretes hundreds of effectors for successful survival in its host plants. The effectors modulate the plant defense system at diverse cellular compartments to take an advantage of pathogen survivals. A few research studies have shown the mode of action of each effector and their interacting proteins in plant cells. Here, we investigated the mode of action of a P. infestans effector, Pi23226, which induces cell death in Nicotiana benthamiana. To identify its host factors, we performed coimmunoprecipitation and liquid chromatography-mass spectrometry, and selected members of heat shock protein 70 (HSP70s) as candidates. These HSP70s, known to function as chaperones, were associated with Pi23226 in planta and accelerated Pi23226-induced cell death. Additionally, they were found to be involved in plant basal defense by suppressing the growth of P. infestans. We also found that specific components of a mitogen-activated protein kinase cascade were involved in Pi23226-induced cell death. Our findings show that HSP70s functions in defense systems by regulating effector-triggered cell death and by suppressing the growth of the pathogen. This suggests that host plants manipulate the ubiquitous proteins to detect pathogen effectors for functioning in the defense system.

摘要

一种具有破坏性的病原体,致病疫霉,分泌了数百种效应物,以在其宿主植物中成功生存。这些效应物在不同的细胞区室中调节植物防御系统,以利用病原体的存活。一些研究表明了每个效应物及其在植物细胞中的相互作用蛋白的作用模式。在这里,我们研究了一种诱导本氏烟细胞死亡的致病疫霉效应物 Pi23226 的作用模式。为了鉴定其宿主因子,我们进行了共免疫沉淀和液相色谱-质谱分析,选择热休克蛋白 70(HSP70)家族成员作为候选物。这些 HSP70 已知作为伴侣发挥作用,与 Pi23226 一起在植物体内,并加速 Pi23226 诱导的细胞死亡。此外,它们被发现通过抑制致病疫霉的生长参与植物基础防御。我们还发现,丝裂原活化蛋白激酶级联的特定成分参与了 Pi23226 诱导的细胞死亡。我们的研究结果表明,HSP70 通过调节效应物触发的细胞死亡和抑制病原体的生长,在防御系统中发挥作用。这表明宿主植物操纵普遍存在的蛋白质来检测病原体效应物,以在防御系统中发挥作用。

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