Smoking out the masters: transcriptional regulators for nicotine biosynthesis in tobacco

概要

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Nicotine and tropane alkaloids are specialized metabolites produced in certain species of Solanaceae, and some of these alkaloids have been used as pharmacological agents. In tobacco plants, nicotine is a defensive toxin against herbivorous insects, and jasmonate (JA) signaling leads to the induction of nicotine biosynthesis. JA-responsive structural genes of the nicotine pathway have been identified as being down-regulated in a low-nicotine tobacco mutant, which possesses mutant alleles at two loci, NICOTINE1 and NICOTINE2 (NIC1 and NIC2). A group of JA-responsive genes that encode homologous ERF transcription factors are clustered at the NIC2 locus and deleted in the mutant. These NIC2-locus ERFs up-regulate the structural genes of the biosynthetic pathway by recognizing GCC-like boxes in their promoters, forming a regulon for nicotine biosynthesis with the downstream targeted genes. The three basic components in JA signaling, COI1, JAZ, and MYC2, are required for JA-induced nicotine formation in tobacco. The bHLH transcription factor MYC2 positively regulates the structural genes, both directly by recognizing G boxes in their promoters and indirectly by up-regulating NIC2-locus ERF genes. Molecular elucidation of nicotine regulation would lead us to better understand the JA-dependent regulation of a wide range of phytochemicals.