Ethylene represses jasmonate signaling to attenuate nicotine biosynthesis in Nicotiana tabacum

It has been known for many years that ethylene represses Jasmonic acid (JA)-induced nicotine biosynthesis. However, it is unclear whether ethylene (ET) alone can inhibit nicotine biosynthesis, and if so, how it achieves this. In this study, we found that ethylene alone can suppress nicotine accumulation and the expression of nicotine biosynthesis and transport genes in tobacco. We then performed transcriptome analysis to explore the underlying molecular mechanism. Results showed that over 6000 differentially expressed genes (DEGs) after 2, 4, 8 and 24 h treatment of ethephon, an ethylene-releasing compound, were identified. GO and KEGG enrichment analysis revealed that DEGs were enriched in pathways related to nicotine biosynthesis, including “pyridine nucleotide metabolic process” and “pyridine-containing compound metabolic process” 4 h after ethephon treatment. Further analysis revealed that expression of key regulators of JA-mediated nicotine biosynthesis was significantly altered by ethephon treatment. Specifically, CORONATINE-INSENSITIVE 1 (COI1) genes COI1 / COI1L and ETHYLENE RESPONSE FACTOR (ERF) genes ERF189 / 199 , which are two major positive regulators of nicotine biosynthesis, were downregulated, whereas four JASMONATE-ZIM-DOMAIN (JAZ) genes JAZ1 / 2b / 7a / 10 were upregulated, indicating that ET suppresses nicotine biosynthesis, at least in part, by repressing the JA signaling pathway. In addition, we identified a set of ET-responsive candidate regulatory genes co-expressed with ERF189 / 199 , providing a resource for future functional studies of nicotine biosynthesis regulation in tobacco roots.