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The Plant Cell, Vol. 14, 979-992, May 2002, Copyright © 2002,
American Society of Plant Biologists

Arabidopsis RAR1 Exerts Rate-Limiting Control of R Gene–Mediated Defenses against Multiple Pathogens

Paul R. Musketta, Katherine Kahna, Mark J. Austina, Lisa J. Moisana, Ari Sadanandoma, Ken Shirasua, Jonathan D. G. Jonesa and Jane E. Parker1,a,b

a The Sainsbury Laboratory, John Innes Centre, Colney, Norwich NR4 7UH, United Kingdom
b Department of Molecular Plant Pathology, Max-Planck-Institute for Plant Breeding Research, Carl-von-Linné-Weg 10, D-50829 Cologne, Germany

1 To whom correspondence should be addressed. E-mail parker{at}mpiz-koeln.mpg.de; fax 49-221-5062353

We have identified the Arabidopsis ortholog of barley RAR1 as a component of resistance specified by multiple nucleotide binding/Leu-rich repeat resistance (R) genes recognizing different bacterial and oomycete pathogen isolates. Characterization of partially and fully defective rar1 mutations revealed that wild-type RAR1 acts as a rate-limiting regulator of early R gene–triggered defenses, determining the extent of pathogen containment, hypersensitive plant cell death, and an oxidative burst at primary infection sites. We conclude that RAR1 defense signaling function is conserved between plant species that are separated evolutionarily by 150 million years. RAR1 encodes a protein with two zinc binding (CHORD) domains that are highly conserved across eukaryotic phyla, and the single nematode CHORD-containing homolog, Chp, was found previously to be essential for embryo viability. An absence of obvious developmental defects in null Arabidopsis rar1 mutants favors the notion that, in contrast, RAR1 does not play a fundamental role in plant development.




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