植物免疫性往往通過(guò)相應(yīng)的植物抗性蛋白 (R) 來(lái)識(shí)別病原體編碼的無(wú)毒因素,，從而引發(fā)過(guò)敏性反應(yīng) (HR) ，使感染的地方形成壞死病灶來(lái)限制病原的擴(kuò)散,。
擬南芥抗性蛋白 (HRT) 能夠抵抗蕪菁皺病毒 (TCV) 的感染,。在篩選識(shí)別蕪菁皺病毒的無(wú)毒缺陷突變體的過(guò)程中，Kang等人發(fā)現(xiàn)了識(shí)別蕪菁皺病毒的缺陷突變體 (CRT1) 可以在早期終止一個(gè)ATP酶蛋白,。如果已經(jīng)感染了蕪菁皺病毒,，CRT1引發(fā)的過(guò)敏性反應(yīng)不能控制病毒復(fù)制和擴(kuò)散，則CRT1還可以抑制ssi4誘導(dǎo)的類HR細(xì)胞的死亡,，其中ssi4是一種由丁香假單胞菌攜帶的avrrpt2抗性蛋白,。此外，CRT1與HRT,、ssi4,，以及其它兩個(gè)抗性蛋白（RPS2和RX）相互作用共同抑制蕪菁皺病毒的感染。
該研究表明,，CRT1是抗性蛋白發(fā)出防御信號(hào)的重要媒介,。相關(guān)論文發(fā)表在2008年1月17日的《細(xì)胞—宿主與微生物》（Cell Host & Microbe）雜志上。（科學(xué)網(wǎng) 武彥文/編譯）
生物谷推薦原始出處：
Cell Host and Microbe, Vol 3, 48-57, 17 January 2008
Article
CRT1, an Arabidopsis ATPase that Interacts with Diverse Resistance Proteins and Modulates Disease Resistance to Turnip Crinkle Virus
Hong-Gu Kang,1 Joseph C. Kuhl,1,3 Pradeep Kachroo,2 and Daniel F. Klessig1,
1 Boyce Thompson Institute for Plant Research, Ithaca, NY 14853, USA
2 Department of Plant Pathology, University of Kentucky, Lexington, KY 40546, USA
Corresponding author
Daniel F. Klessig
[email protected]
Summary
Plant immunity frequently involves the recognition of pathogen-encoded avirulence (avr) factors by their corresponding plant resistance (R) proteins. This triggers the hypersensitive response (HR) where necrotic lesions formed at the site(s) of infection help restrict pathogen spread. HRT is an Arabidopsis R protein required for resistance to turnip crinkle virus (TCV). In a genetic screen for mutants compromised in the recognition of TCV's avr factor, we identified crt1 (compromised recognition of TCV), a mutant that prematurely terminates an ATPase protein. Following TCV infection, crt1 developed a spreading HR and failed to control viral replication and spread. crt1 also suppressed HR-like cell death induced by ssi4, a constitutively active R protein, and by Pseudomonas syringae carrying avrRpt2. Furthermore, CRT1 interacts with HRT, SSI4, and two other R proteins, RPS2 and Rx. These data identify CRT1 as an important mediator of defense signaling triggered by distinct classes of R proteins.
