CRT1, an Arabidopsis ATPase that Interacts with Diverse Resistance Proteins and Modulates Disease Resistance to Turnip Crinkle Virus

Hong Gu Kang; Joseph C. Kuhl; Pradeep Kachroo; Daniel F. Klessig

doi:10.1016/j.chom.2007.11.006

CRT1, an Arabidopsis ATPase that Interacts with Diverse Resistance Proteins and Modulates Disease Resistance to Turnip Crinkle Virus

Hong Gu Kang, Joseph C. Kuhl, Pradeep Kachroo, Daniel F. Klessig

Plant Pathology

Research output: Contribution to journal › Article › peer-review

67 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	48-57
Number of pages	10
Journal	Cell Host and Microbe
Volume	3
Issue number	1
DOIs	https://doi.org/10.1016/j.chom.2007.11.006
State	Published - Jan 17 2008

Bibliographical note

Funding 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).

Funding

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).

Funders	Funder number
Directorate for Biological Sciences	0641576
U.S. Department of Agriculture

Keywords

MICROBIO
MOLIMMUNO

ASJC Scopus subject areas

Parasitology
Microbiology
Virology

Access to Document

10.1016/j.chom.2007.11.006

Cite this

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title = "CRT1, an Arabidopsis ATPase that Interacts with Diverse Resistance Proteins and Modulates Disease Resistance to Turnip Crinkle Virus",

abstract = "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.",

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note = "Funding 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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AU - Kachroo, Pradeep

AU - Klessig, Daniel F.

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N2 - 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.

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