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First published online April 29, 2002; 10.1105/tpc.001032

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The Plant Cell, Vol. 14, 1005-1015, May 2002, Copyright © 2002,
American Society of Plant Biologists

RAR1 and NDR1 Contribute Quantitatively to Disease Resistance in Arabidopsis, and Their Relative Contributions Are Dependent on the R Gene Assayed

Pablo Torneroa, Peter Merrittb, Ari Sadanandomc, Ken Shirasuc, Roger W. Innesb and Jeffery L. Dangl1,a,d

a Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599
b Department of Biology, Indiana University, Bloomington, Indiana 47405
c Sainsbury Laboratory, John Innes Centre, Colney, Norwich NR4 7UH, United Kingdom
d Department of Microbiology and Immunology and Curriculum in Genetics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599

1 To whom the correspondence should be addressed. E-mail dangl{at}email.unc.edu; fax 919-962-1625

Plant disease resistance (R) genes mediate specific pathogen recognition, leading to a successful immune response. Downstream responses include ion fluxes, an oxidative burst, transcriptional reprogramming, and, in many cases, hypersensitive cell death at the infection site. We used a transgenic Arabidopsis line carrying the bacterial avirulence gene avrRpm1 under the control of a steroid-inducible promoter to select for mutations in genes required for RPM1-mediated recognition and signal transduction. We identified an allelic series of eight mutants that also were allelic to the previously identified pbs2 mutation. Positional cloning revealed this gene to be AtRAR1, the Arabidopsis ortholog of barley RAR1, a known mediator of R function. AtRAR1 is required for both full hypersensitive cell death and complete disease resistance mediated by many, but not all, tested R genes. Double mutant analysis of Atrar1 in combination with the R signal intermediate ndr1 suggests that AtRAR1 and NDR1 can operate in both linear and parallel signaling events, depending on the R gene function triggered. In Atrar1 null plants, the levels of RPM1-myc are reduced severely, suggesting that AtRAR1 may regulate R protein stability or accumulation.




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