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.
|Number of pages||10|
|Journal||Cell Host and Microbe|
|State||Published - Jan 17 2008|
Bibliographical noteFunding Information:
We thank Dr. Moffett for the HRT, Rx, SNC, N, GFP constructs and stimulating discussion, Drs. Staskawicz and Katagiri for the RPS2 constructs, Dr. Dempsey for critical comments on the manuscript, and Ms. Kim and Drs. Park, Rairdan, Sacco, and Bhattacharjee for assistance and advice. This work was supported by grants from USDA (2003-35319-13312) and NSF (IOS-0641576).
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