2009年7月23日，我所張躍林實(shí)驗(yàn)室在Cell Host & Microbe雜志上發(fā)表題為“Regulation of Cell Death and Innate Immunity by Two Receptor-like Kinases in Arabidopsis”的文章,。該文章報(bào)道了受體類(lèi)蛋白激酶BIR1對(duì)分別依賴(lài)于PAD4和SOBIR1的兩條植物先天性免疫反應(yīng)信號(hào)通路的負(fù)調(diào)控機(jī)制。
受體類(lèi)蛋白激酶BAK1在調(diào)控植物發(fā)育和先天性免疫反應(yīng)中發(fā)揮了重要的作用,。運(yùn)用反向遺傳學(xué)技術(shù)，我們分離到一株T-DNA插入突變體bir1-1,，表現(xiàn)出植株矮小,、苗期死亡的表型。BIR1的突變導(dǎo)致植物先天性免疫反應(yīng)的激活,。BIR1與BAK1在細(xì)胞膜上形成蛋白復(fù)合物,。雙突變體bak1bkk1的表型與bir1-1極為相似。PAD4和EDS1的突變可以部分抑制bir1-1的表型,，而EDS5,、SID2和NDR1對(duì)bir1-1的表型也有一定的調(diào)控作用。為了進(jìn)一步分析bir1-1激活的信號(hào)通路,，用EMS對(duì)bir1-1進(jìn)行遺傳誘變,，我們克隆了bir1-1的一個(gè)抑制突變體（sobir1-1）。SOBIR1 對(duì)bir1-1的表型是必需的,，SOBIR1和PAD4的同時(shí)突變可以完全抑制bir1-1的表型,。SOBIR1編碼一個(gè)受體類(lèi)蛋白激酶,。過(guò)量表達(dá)SOBIR1會(huì)導(dǎo)致植物自發(fā)性的細(xì)胞死亡,，對(duì)病原菌的抗性大大增強(qiáng)。說(shuō)明SOBIR1正調(diào)控植物的抗病反應(yīng),。這些研究結(jié)果表明BIR1在依賴(lài)于SOBIR1和PAD4的兩條信號(hào)通路中發(fā)揮了負(fù)調(diào)控作用,。（生物谷Bioon.com）
生物谷推薦原始出處：
Cell Host & Microbe, Volume 6, Issue 1, 34-44, 23 July 2009 doi:10.1016/j.chom.2009.05.019
Regulation of Cell Death and Innate Immunity by Two Receptor-like Kinases in Arabidopsis
Minghui Gao1,2,Xia Wang2,Dongmei Wang3,4,Fang Xu2,Xiaojun Ding2,Zhibin Zhang2,Dongling Bi2,Yu Ti Cheng3,She Chen2,Xin Li3andYuelin Zhang2,,
1 College of Biological Sciences, China Agricultural University, Beijing 100094, China
2 National Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing 102206, China
3 Michael Smith Laboratories, University of British Columbia, Vancouver V6T 1Z4, Canada
Upon recognition of bacterial flagellin, the plant receptor FLS2 heterodimerizes with brassinosteroid insensitive 1-associated receptor kinase 1 (BAK1) and activates plant defense responses. Because constitutive activation of defense responses is detrimental, plant resistance signaling pathways must benegatively controlled, although the mechanisms involved are unclear. We identified Arabidopsis BIR1 as a BAK1-interacting receptor-like kinase. Knocking out BIR1 leads to extensive cell death, activation of constitutive defense responses, and impairment in the activation of MPK4, a negative regulator of plant resistance (R) protein signaling, by flagellin. sobir1-1, a mutant obtained in a screen for suppressors of the bir1-1 phenotype, rescued cell death observed in bir1-1. SOBIR1 encodes another receptor-like kinase whose overexpression activates cell death and defense responses. Our data suggest that BIR1 negatively regulates multiple plant resistance signaling pathways, one of which is the SOBIR1-dependent pathway identified here.
