2010年4月22日,，NIBS周儉民實(shí)驗(yàn)室在Cell Host & Microbe雜志發(fā)表最新論文。論文報(bào)道了一類寄主胞質(zhì)內(nèi)受體類似激酶是植物天然免疫信號(hào)傳導(dǎo)的新的重要元件,。
由植物細(xì)胞膜受體感受病原相關(guān)分子模式激活的免疫反應(yīng)（PTI）對(duì)植物不可或缺。致病微生物常常通過(guò)向寄主細(xì)胞內(nèi)分泌一些效應(yīng)蛋白來(lái)抑制PTI信號(hào)傳導(dǎo),，從而促進(jìn)病原菌的侵染和增殖,。隨后植物進(jìn)化出抗性蛋白特異地識(shí)別某些病原菌的效應(yīng)蛋白再度激活免疫反應(yīng)（ETI）。攜帶抗病蛋白R(shí)PS5的植物能特異識(shí)別丁香假單胞菌的效應(yīng)蛋白AvrPphB,。
AvrPphB是一個(gè)半胱氨酸蛋白酶,，RPS5在非激活狀態(tài)時(shí)與一個(gè)叫PBS1的蛋白激酶形成復(fù)合體，后者通過(guò)被AvrPphB切割導(dǎo)致RPS5發(fā)生構(gòu)象變化從而變?yōu)榧せ顮顟B(tài),。本文發(fā)現(xiàn)AvrPphB的原始功能很可能是通過(guò)降解與PBS1類似的激酶（PBL）從而抑制PTI來(lái)幫助細(xì)菌侵染的,。研究表明，與PBS1同源的BIK1和PBL1在多條PTI信號(hào)通路中起關(guān)鍵作用,。它們直接與植物細(xì)胞表面受體偶聯(lián),，激活胞內(nèi)信號(hào)通路。推測(cè)PBS1是從PBL家族中演化而來(lái),，特異性地識(shí)別AvrPphB從而激活ETI,。這一發(fā)現(xiàn)不僅增進(jìn)了人們對(duì)植物PTI信號(hào)傳導(dǎo)機(jī)理的認(rèn)識(shí)，同時(shí)還為ETI的進(jìn)化方式提供了證據(jù),。
NIBS博士后張杰與技術(shù)員李魏為本文的共同第一作者,，論文的其他作者還有NIBS博士生向婷婷，技術(shù)員劉自旭,，Purdue University的研究生Kristin Laluk和Tesfaye Mengiste博士, NIBS技術(shù)員丁曉軍,張曉娟,已畢業(yè)博士生鄒燕,高明輝,以及陳涉博士和張躍林博士,。周儉民博士為本文的通訊作者。此項(xiàng)研究由科技部863和北京市科委資助,，在北京生命科學(xué)研究所完成,。
Michigan State University的Brad Day博士和Sheng Yang He博士在Cell Host & Microbe雜志為該論文配發(fā)了題為“Battling immune kinases in plants”的點(diǎn)評(píng)，指出該工作為PTI和ETI在進(jìn)化上相互關(guān)聯(lián)提供了強(qiáng)有力的證據(jù),。相關(guān)報(bào)道見 ｈｔｔｐ://ｗｗｗ.ｃｅｌｌ.ｃｏｍ/ｃｅｌｌ-ｈｏｓｔ-ｍｉｃｒｏｂｅ/ａｂｓｔｒａｃｔ/Ｓ１９３１-３１２８(１０)００１０９-５ ,。（生物谷Bioon.com）
生物谷推薦原文出處：
Cell Host & Microbe doi:10.1016/j.chom.2010.03.007
Receptor-like Cytoplasmic Kinases Integrate Signaling from Multiple Plant Immune Receptors and Are Targeted by a Pseudomonas syringae Effector
Jie Zhang1, 4, Wei Li1, 4, Tingting Xiang1, 2, Zixu Liu1, Kristin Laluk3, Xiaojun Ding1, Yan Zou1, Minghui Gao1, Xiaojuan Zhang1, She Chen1, Tesfaye Mengiste3, Yuelin Zhang1 and Jian-Min Zhou1, ,
1 National Institute of Biological Sciences, Beijing 102206, China
2 State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing 100094, China
3 Department of Botany and Plant Pathology, Purdue University, West Lafayette, IN 47907, USA
Cell-surface-localized plant immune receptors, such as FLS2, detect pathogen-associated molecular patterns (PAMPs) and initiate PAMP-triggered immunity (PTI) through poorly understood signal-transduction pathways. The pathogenic Pseudomonas syringae effector AvrPphB, a cysteine protease, cleaves the Arabidopsis receptor-like cytoplasmic kinase PBS1 to trigger cytoplasmic immune receptor RPS5-specified effector-triggered immunity (ETI). Analyzing the function of AvrPphB in plants lacking RPS5, we find that AvrPphB can inhibit PTI by cleaving additional PBS1-like (PBL) kinases, including BIK1, PBL1, and PBL2. In unstimulated plants, BIK1 and PBL1 interact with FLS2 and are rapidly phosphorylated upon FLS2 activation by its ligand flg22. Genetic and molecular analyses indicate that BIK1, and possibly PBL1, PBL2, and PBS1, integrate immune signaling from multiple immune receptors. Whereas AvrPphB-mediated degradation of one of these kinases, PBS1, is monitored by RPS5 to initiate ETI, this pathogenic effector targets other PBL kinases for PTI inhibition.
