GENETIC DISSECTION OF THE RPS5 DISEASE RESISTANCE PATHWAY IN ARABIDOPSIS
RF WARREN1, PM MERRITT1, A HENK1, E HOLUB2 and RW INNES1
1Department of Biology, Indiana University, Bloomington, IN 47405, USA; 2Horticulture Research lnternational - Wellesbourne, Warwickshire CV35 9EF, UK
Background and objectives
The signal transduction pathways that lead from pathogen recognition to activation of defence responses in plants are poorly understood. To genetically dissect these pathways we screened for mutations in Arabidopsis that block or alter defence responses mediated by the RPS5 disease resistance gene. RPS5 confers resistance to strains of Pseudomonas syringae that carry the avirulence gene avrPphB .
Results and conclusions
We isolated six mutants that displayed enhanced susceptibility to P. syringae strains that carry avrPphB. Genetic complementation analyses revealed that two of these were rps5 mutants, while the remaining four defined three additional genes, which we have designated PBS1, PBS2 and PBS3. Mutations in PBS1 reduce resistance mediated by RPS5, but do not affect resistance mediated by other disease-resistance genes in Arabidopsis, indicating that the PBS1 protein functions in a pathway specific to RPS5, potentially interacting with RPS5 and/or AvrPphB. In contrast to PBS1, mutations in PBS2 and PBS3 affect several Arabidopsis disease-resistance gene pathways, including resistance genes specific to the oomycete pathogen Peronospora parasitica. The pbs3 mutation appears to suppress induction of systemic acquired resistance as induction of the SAR-associated gene PR-1 by both virulent and avirulent pathogens is dramatically reduced, while induction of PR-1 by salicylic acid is not affected. Interestingly, the rps5-1 mutation also affects multiple disease-resistance gene pathways. We have isolated RPS5 and determined that it is a member of the NBS-LRR family of disease resistance genes. The rps5-1 mutant contains a single amino-acid substitution in the third LRR of RPS5, suggesting that this region may physically interact with a signal transduction component shared by other disease-resistance gene pathways.
Funding for this project was provided by the National Institute of General Medical Sciences grant R01GM46451 to RWI.
1. Simonich MT, lnnes RW, 1995. Molecular Plant-Microbe Interactions 8, 637-640.