Constitutive salicylic acid-dependent signaling in cpr1 and cpr6 mutants requires PAD4

Salicylic acid (SA)-dependent signaling controls activation of a set of pla nt defense mechanisms that are important for resistance to a variety of mic robial pathogens. Many Arabidopsis mutants that display altered SA-dependen t signaling have been isolated. We used double mutant analysis to determine the relative positions of the pad4, cpr1, cpr5, cpr6, dnd1 and dnd2 mutati ons in the signal transduction network leading to SA-dependent activation o f defense gene expression and disease resistance. The pad4 mutation causes failure of SA accumulation in response to infection by certain pathogens, w hile the other mutations cause constitutively high levels of SA, defense ge ne expression and resistance. The cpr7 pad4, cpr5 pad4, cpr6 pad4, dnd1 pad 4 and dnd2 pad4 double mutants were constructed and assayed for stature, pr esence of spontaneous lesions, resistance to Pseudomonas syringae and Peron ospora parasitica, SA levels, expression of PAD4 PR-I and PDF1.2 and accumu lation of camalexin. We found that the effects of the cpr1 and cpr6 mutatio ns on SA-dependent gene expression are completely dependent on PAD4 functio n. In contrast, SA accumulation in the lesion-mimic mutant cpr5 is partiall y PAD4-independent, while in dnd1 and dnd2 mutants it is completely PAD4-in dependent. A model describing a possible arrangement of activities in the s ignal transduction network is presented.