Constitutive disease resistance requires EDS1 in the Arabidopsis mutants cpr1 and cpr6 and is partially EDS1-dependent in cpr5

The systemic acquired resistance (SAR) response in Arabidopsis is character ized by the accumulation of salicylic acid (SA), expression of the pathogen esis-related (PR) genes, and enhanced resistance to virulent bacterial and oomycete pathogens. The cpr (constitutive expressor of PR genes) mutants ex press all three SAR phenotypes. In addition, cpr5 and cpr6 induce expressio n of PDF1.2 a defense-related gene associated with activation of the jasmon ate/ethylene-mediated resistance pathways, cpr5 also forms spontaneous lesi ons. In contrast, the eds7 (enhanced disease susceptibility) mutation aboli shes race-specific resistance conferred by a major subclass of resistance ( R) gene products in response to avirulent pathogens. eds7 plants also exhib it increased susceptibility to virulent pathogens. Epistasis experiments we re designed to explore the relationship between the cpr- and EDS1-mediated resistance pathways. We found that a null eds7 mutation suppresses the dise ase resistance phenotypes of both cpr1 and cpr6. In contrast, eds1 only par tially suppresses resistance in cpr5, leading us to conclude that cpr5 expr esses both EDS1-dependent and EDS1-independent components of plant disease resistance. Although eds1 does not prevent lesion formation on cpr5 leaves, it alters their appearance and reduces their spread. This phenotypic diffe rence is associated with increased pathogen colonization of cpr5 eds1 plant s compared to cpr5. The data allow us to place EDS1 as a necessary downstre am component of cpr1- and cpr6-mediated responses, but suggest a more compl ex relationship between EDS1 and cpr5 in plant defense.