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

Author
item KANG, HONG-GU - BOYCE THOMPSON INSTITUTE
item KUHL, JOSEPH
item KACHROO, PRADEEP - UNIV. OF KENTUCKY
item KLESSIG, DANIEL - BOYCE THOMPSON INSTITUTE

Submitted to: Cell Host and Microbe
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/15/2007
Publication Date: 1/20/2008
Citation: Kang, H., Kuhl, J.C., Kachroo, P., Klessig, D.F. 2008. CRT1, an Arabidopsis ATPase that Interacts with Diverse Resistance Proteins and Modulates Disease Resistance to Turnip Crinkle Virus. Cell Host and Microbe. 3:48-57.

Interpretive Summary: Dijon, an ecotype of the common weed known as wall cress, was used to study plant resistance to turnip crinkle virus (TCV). Previously, it had been shown that the resistance gene HRT was necessary for cell death leading to resistance in the presence of TCV. The TCV coat protein (CP) is necessary for starting plant resistance. Mutation was used to identify a line (crt1, compromised recognition of TCV) that showed limited recognition of the TCV CP. This mutation occurred in an ATPase protein. In crt1 plants the TCV CP did not cause cell death. However, infection with TCV triggers cell death and disease development occurs. The crt1 mutation also affects a plant’s resistance response related to a bacterial pathogen. The CRT1 gene may be important for many types of plant resistance which will help develop resistant crops leading to healthy plants without applying as many chemicals.

Technical Abstract: HRT is a CC-NBS-LRR-type resistance (R) protein that is required for resistance to turnip crinkle virus (TCV) in Arabidopsis. To gain insights into HRT-mediated signaling, a genetic screen was performed to identify mutants compromised for recognition of the TCV avirulence factor, which was encoded by an endogenously expressed TCV coat protein (CP) transgene. One mutant, crt1 (compromised recognition of TCV), was identified; the crt1 mutation causes premature termination of a novel ATPase protein, leading to deletion of a recently recognized GHKL ATPase motif termed a ‘Bergerat fold’. While crt1 plants did not display cell death in response to expression of a CP transgene, they developed a hypersensitive response (HR) following TCV infection. At early times after infection, HR development in crt1 and TCV-resistant Di-17 plants was comparable; however, the lesions formed by crt1 plants continued to spread and eventually covered the entire leaf, whereas those on Di-17 plants remained discrete. crt1 plants also were compromised for TCV resistance, as they allowed systemic viral movement and developed disease symptoms, including chlorosis, diminished numbers and length of bolts and reduced seed set. These symptoms were even more pronounced when the two mostly closely related CRT1 homologs were partially silenced. In addition, silencing CRT1 and its homologs in the Col-0 background led to delayed HR against avirulent Pseudomonas syringae carrying avrRpt2 and the crt1 mutation partially suppressed spontaneous cell death in the ssi4 mutant, which contains a gain-of-function mutation in a TIR-NBS-LRR type R gene. In summary, this novel CRT1 family appears to play an important function in activating defenses against pathogen infection.