March
2005
, Volume
18
, Number
3
Pages
212
-
219
Authors
John
Cawly
,
1
Anthony B.
Cole
,
1
Lóránt
Király
,
2
Wenping
Qiu
,
3
and
James E.
Schoelz
1
Affiliations
1Department of Plant Microbiology and Pathology, University of Missouri, Columbia, MO 65211, U.S.A.; 2Plant Protection Institute, Hungarian Academy of Sciences, P.O. Box 102, 1525 Budapest, Hungary; 3Department of Fruit Science, Southwest Missouri State University, Mountain Grove, MO 65711, U.S.A.
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RelatedArticle
Accepted 3 November 2004.
Abstract
The P6 protein of Cauliflower mosaic virus (CaMV) W260 elicits a hypersensitive response (HR) on inoculated leaves of Nicotiana edwardsonii. This defense response, common to many plant pathogens, has two key characteristics, cell death within the initially infected tissues and restriction of the pathogen to this area. We present evidence that a plant gene designated CCD1, originally identified in N. bigelovii, can selectively block the cell death pathway during HR, whereas the resistance pathway against W260 remains intact. Suppression of cell death was evident not only macroscopically but also microscopically. The suppression of HR-mediated cell death was specific to CaMV, as Tobacco mosaic virus was able to elicit HR in the plants that contained CCD1. CCD1 also blocks the development of a systemic cell death symptom induced specifically by the P6 protein of W260 in N. clevelandii. Introgression of CCD1 from N. bigelovii into N. clevelandii blocked the development of systemic cell death in response to W260 infection but could not prevent systemic cell death induced by Tomato bushy stunt virus. Thus, CCD1 blocks both local and systemic cell death induced by P6 of W260 but does not act as a general suppressor of cell death induced by other plant viruses. Furthermore, experiments with CCD1 provide further evidence that cell death could be uncoupled from resistance in the HR of Nicotiana edwardsonii to CaMV W260.
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© 2005 The American Phytopathological Society