Figure 10

The signaling network for interactions among SA, JA, ethylene and ROS that modulate defense activation or development of cell death. a, SA inhibits apoplastic ROS signaling and expression of defense genes. Mutants with elevated SA accumulation display constitutive expression of defense related genes and an attenuated O₃ gene expression response. Simultaneously abolishing SA dependent and independent signaling components (ALD1, SID2, EDS1) in dnd1 restore its response to ozone. Moreover, pretreatment of wildtype with SA leads to a reduced response to ozone. b, SA-dependent and SA-independent signaling components synergistically regulate development of cell death. The exact function of DND1 function in cell death still remains to be determined, but it is likely that high SA concentration in this mutant contributes to cell death. Consequently, a mutation in SID2 can significantly reduce the amount of SA accumulation and cell death in dnd1. ALD1 and FMO1 are required for Pip induced SAR and SA accumulation in systemic tissues and appears to synergistically regulate cell death and defense response with SA. Moreover, EDS1 affects the onset of SA synthesis and can also directly regulate cell death. Abolishing JA in dnd1sid2 double mutant strengthened cell death suggested that there is the anti-death regulatory function of JA signaling either through JA-SA interaction or unknown signaling components.