The disease resistance signaling components EDS1 and PAD4 are essential regulators of the cell death pathway controlled by LSD1 in arabidopsis

Specific recognition of pathogens is mediated by plant disease resistance ( R) genes and translated into a successful defense response. The extent of a ssociated hypersensitive cell death varies from none to an area encompassin g cells surrounding an infection site, depending on the R gene activated. W e constructed double mutants in Arabidopsis between positive regulators of R function and a negative regulator of cell death, LSD1, to address whether genes required for normal R function also regulate the runaway cell death observed in lsd1 mutants. We report here that EDS1 and PAD4, two signaling genes that mediate some but not all R responses, also are required for runa way cell death in the lsd1 mutant. Importantly, this novel function of EDS1 and PAD4 is operative when runaway cell death in lsd1 is initiated through an R gene that does not require EDS1 or PAD4 for disease resistance. NDR1, another component of R signaling, also contributes to the control of plant cell death. The roles of EDS1 and PAD4 in regulating lsd1 runaway cell dea th are related to the interpretation of reactive oxygen intermediate-derive d signals at infection sites. We further demonstrate that the fate of super oxide at infection sites is different from that observed at the leading mar gins of runaway cell death lesions in lsd1 mutants.