| In plants, specific recognition of pathogens, mediated by disease resistance (R) genes, initiates successful defense responses. Among these responses is a plant programmed cell death termed the hypersensitive response. Several features of R-dependent signaling suggest that negative regulation of the hypersensitive response is an important factor limiting the spread of unnecessary cell death. This implies that there should be an interaction between genes positively regulating R-dependent responses and those mediating negative control of unwanted cell death. To test this model, I constructed double mutants between plants impaired for two positive regulators of R function and plants mutated for a key negative regulator of cell death, LSD1. I also constructed double mutants between lsd1 and two known mediators of many disease resistance responses. lsd1 plants display a characteristic runaway cell death phenotype in response to multiple biotic and abiotic stimuli. Furthermore, lsd1 have an enhanced basal resistance providing these plants with resistance to normally virulent pathogens on wild type. I found that EDS1 and PAD4, mediators of some but not all R responses, have a second function required to trigger the negative regulatory function of LSD1 which controls runaway cell death. These ancillary functions of genes required for R function are related to interpretation of reactive oxygen intermediate signals at infection sites. Furthermore, the enhanced basal resistance functioning in lsd1 mutants requires both EDS1 and PAD4. I also found that salicylic acid accumulation (SA) and NIM1, both required for many resistance responses including systemic acquired resistance, are also required for lsd1 -mediated runaway cell death. SA application triggers runaway cell death in lsd1, but not wild type plants. SA is also required for runaway cell death in lsd1 plants. Therefore SA is both necessary for the initiation and the perpetuation of lsd1 cell death. I also determined that SA accumulation and NIM1 are not required for the basal resistance functioning in lsd1 plants. These results demonstrate the dual nature of the lsd1 phenotype by separating lsd1 runaway cell death from lsd1 basal resistance. |
