Abstract
Nicotine-biosynthesis genes are mainly expressed in tobacco roots and their expression is enhanced by methyl jasmonic acid (MeJA). Study using tobacco low-nicotine nic mutants have revealed that expression of nicotine-biosynthesis genes is positively regulated by NIC loci and that the JA cascade modulating nicotine-biosynthesis works NIC loci-dependently. Because NIC loci partially function in MeJA-treated leaves, we compared the mRNA population in the MeJA-treated leaves of wild-type tobacco and those of the corresponding low-nicotine nic mutant by differential display to survey genes involved in NIC-dependent JA-response. A cDNA showing NIC-dependent and JA-induced expression was isolated, and its corresponding gene was named as JEI1. Wounding enhances the JEI1 expression in the leaves rapidly and transiently as well as MeJA. Treatment with elicitors and protein synthesis inhibitor also increases JEI1 transcript level. The protein encoded by JEI1 is a novel protein that has two protein-protein interacting domains.
