The Jasmonic Acid/Ethylene-Activated Signaling Cascade

Jasmonic acid (JA) and its derivative Jasmonoyl-isoleucine (JA-Ile) accumulate upon wounding (e.g. herbivory) and upon attack with necrotrophic pathogens. However, different responses are elicited depending on whether the plant is injured by insects or whether it is infected by a pathogen. This differential reaction is due to higher synthesis of ethylene (ET) after pathogen attack than after herbivory (de Vos et al., 2005). The interplay of both pathways is shown below.

The JA pathway is activated through COI1 leading to the degradation of JAZ repressor proteins. JAZ repressors do not only repress MYC2, but also transcription factor EIN3. EIN3 accumulates only when the ET signaling cascade is activated. ET inactivates the ethylene receptor ETR, which represses the ET cascade. Thus, ET induces the cascade finally leading to the stabilization of EIN3. EIN3 activates the promoter of the transcription factor ORA59 which is a master regulator of the JA/ET-activated defense program.

TGA factors are required for the activation of the JA/ET pathway. According to our hypothesis, TGA activity is repressed through an unknown mechanism by plant-specific glutaredoxin ROXY19 which is induced by salicylic acid (SA). This mechanism would explain the observed repression of the JA/ET pathway by SA.