Hypocotyl Elongation Inhibition of Melatonin Is Involved in Repressing Brassinosteroid Biosynthesis in Arabidopsis

Melatonin functions as a plant hormone/regulator in the regulation of growth and development. However, the underlying mechanisms are still unclear. In this study, we found that a high dose of melatonin inhibited hypocotyl elongation in a dose-dependent manner in Arabidopsis. An expression profile analysis showed that hypocotyl growth inhibition by melatonin was involved in reprograming the expression of cell elongation genes and brassinosteroid (BRs) biosynthetic genes. Furthermore, similar to BR biosynthetic inhibitor brassinazole (BRZ), a high concentration of melatonin upregulated BR-biosynthetic genes and downregulated BR-induced genes involved in cell elongation, while melatonin was inefficient in brassinazole-resistant mutants like the bzr1-1D and bes1-D in hypocotyl inhibition. The comparative expression profile analysis showed an opposite expression mode in the co-regulated genes between melatonin and BZR1 or melatonin and brassinolide (BL). Additionally, exogenous BL rescued the repressive phenotype of BR biosynthesis-deficient mutant like det2-1 even in the presence of high-dose melatonin, but not BR receptor mutant bri1-5 or signal transduction mutant bin2-1. A biochemical analysis further confirmed that melatonin reduced endogenous BR levels in a dose-dependent manner in Arabidopsis. Taken together, these results indicate that melatonin inhibits BR biosynthesis but does not block BR signaling in the inhibition of hypocotyl elongation and extends insights on the role of melatonin in cross-talking with plant hormone signaling.