Jasmonate-induced nicotine formation in tobacco is mediated by tobacco COI1 and JAZ genes.

Biosynthesis of many plant alkaloids is enhanced by endogenous accumulation and exogenous application of jasmonates, but the general and specific signaling components are not well understood. In Arabidopsis, jasmonate-induced ZIM-domain-containing (JAZ) proteins have recently been found to be critical transcriptional repressors linking CORONATINE INSENSTIVE1 (COI1)-mediated jasmonate perception and jasmonate-regulated transcriptional regulation. Insect herbivory on tobacco leaves activates the jasmonate signaling pathway, leading to up-regulation of nicotine biosynthesis genes in roots. We show here that roots of COI1-silenced tobacco plants are insensitive to growth inhibition by methyl jasmonate, and do not activate nicotine biosynthesis genes after jasmonate treatment or wounding of leaves. Tobacco JAZ proteins appeared to be rapidly degraded after jasmonate treatment, whereas a C-terminally truncated form lacking the conserved Jas motif did not. When the non-degradable JAZ forms were expressed in tobacco hairy roots, jasmonate induction of nicotine biosynthesis was strongly inhibited. Formation of tobacco alkaloids in jasmonate-elicited tobacco BY-2 cells was also effectively suppressed by the COI1 RNAi (RNA interference) construct and by the dominant-negative truncated JAZ constructs. In addition, jasmonate-mediated induction of nicotine biosynthesis genes was diminished by treatment with a proteasome inhibitor MG132. These results indicate that jasmonate-triggered, COI1-mediated degradation of JAZ repressors activates transcriptional regulation of nicotine biosynthesis genes in tobacco roots.