Long-term methyl jasmonate exposure triggers COI1-independent induction of myrosinases TGG1 and TGG2 in Arabidopsis

Plants are constantly subjected to stresses such as herbivore attacks, which continuously activate the jasmonic acid (JA) signaling pathway in nature. However, knowledge about the effect of long-term activation of the JA signaling pathway on plant defense response remains limited. THIOGLUCOSIDE GLUCOHYDROLASE 1 (TGG1) and TGG2 are enzymes that activate defensive metabolites, namely glucosinolates, which are involved in defense against herbivores and pathogens. Here, we show that prolonged exposure to the wounding hormone methyl jasmonate (MeJA) enhances TGG1 and TGG2 expression in the rosette leaves of 12-d-old Arabidopsis thaliana , and this response does not appear to be strictly dependent on the canonical JA signaling pathway. Airborne MeJA treatment for up to 5 d enhanced both TGG1 and TGG2 gene expression and their protein levels in Arabidopsis leaves. Notably, TGG1 and TGG2 gene expression was also significantly upregulated in two JA signaling pathway mutants, namely coi1–16 and myc2,3,4 , following 5 d of MeJA treatment. TGG1 and TGG2 proteins accumulate in specialized myrosin cells of rosette leaves. Myrosin cell area expanded in response to MeJA treatment in a leaf-age-dependent manner. Consistent with this observation, the expression of FAMA , a transcription factor known to regulate TGG1 and TGG2 expression, was also increased in a leaf-age-dependent manner after 5 d of MeJA treatment. Taken together, our results suggest the existence of additional regulatory mechanisms beyond canonical JA signaling pathway that is activated by long-term exposure to MeJA and regulates the expression of defense-related genes TGG1 and TGG2 .