The Arabidopsis gain-of-function mutant ssi4 requires RAR1 and SGT1b differentially for defense activation and morphological alterations.

ABSTRACT

A gain-of-function mutation in resistance (R) gene SSI4 causes constitutive activation of defense responses, spontaneous necrotic lesion formation, enhanced resistance against virulent pathogens, and a severe dwarf phenotype. Genetic analysis revealed that ssi4-induced H(2)O(2) accumulation and spontaneous cell death require RAR1, whereas ssi4-mediated stunting is dependent on SGT1b. By contrast, both RAR1 and SGT1b are required in a genetically additive manner for ssi4-induced disease resistance, SA accumulation, and lesion formation after pathogen infection. These data point to cooperative yet distinct functions of RAR1 and SGT1b in responses conditioned by a deregulated nucleotide-binding leucine-rich repeat protein. We also found that RAR1 and SGT1b together contribute to basal resistance because an ssi4 rar1 sgt1b triple mutant exhibited enhanced susceptibility to virulent pathogen infection compared with wild-type SSI4 plants. All ssi4-induced phenotypes were suppressed when plants were grown at 22 degrees C under high relative humidity. However, low temperature (16 degrees C) triggered ssi4-mediated cell death via an RAR1-dependent pathway even in the presence of high humidity. Thus, multiple environmental factors impact on ssi4 signaling, as has been observed for other constitutive defense mutants and R gene-triggered pathways.