The role of NDR1 in avirulence gene-directed signaling and control of programmed cell death in Arabidopsis.

Arabidopsis plants containing the ndr1-1 mutation are incapable of mounting a hypersensitive response to bacteria carrying avrRpt2, but show an exaggerated cell death response to bacteria carrying avrB (Century et al., 1995). We show here that ndr1-1 plants are severely impaired in induction of systemic acquired resistance and PR1-driven transcription of a reporter gene in response to Pseudomonas syringae strains carrying avrRpt2 but not in response to P. syringae carrying avrB. The ndr1-1 mutation also impaired salicylic acid (SA) accumulation in response to treatments that produced reactive oxygen species (ROS) and impaired induction of systemic acquired resistance in response to in situ production of ROS. Hydrogen peroxide accumulated in wild-type Arabidopsis leaves beginning 4 to 7 h postinoculation with P. syringae carrying either avrRpt2 or avrB. In ndr1-1 plants, P. syringae carrying avrRpt2 elicited no detectable hydrogen peroxide production. Hydrogen peroxide production in response to bacteria carrying avrB was similar to that of Columbia in kinetics but of lesser intensity at early time points. These data are interpreted to indicate that NDR1 links ROS generation to SA production and that the phenotypic consequences of the ndr1-1 mutation are caused by a reduced ability to accumulate SA upon pathogen infection.