Melatonin enhances salt tolerance by promoting MYB108A-mediated ethylene biosynthesis in grapevines

Abstract

The signal molecules melatonin and ethylene play key roles in abiotic stress tolerance. The interplay between melatonin and ethylene in regulating salt tolerance and the underlying molecular mechanism of this interplay remain unclear. Here, we found that both melatonin and 1-aminocyclopropane-1-carboxylic acid (ACC, a precursor of ethylene) enhanced the tolerance of grapevine to NaCl; additionally, ethylene participated in melatonin-induced salt tolerance. Further experiments indicated that exogenous treatment and endogenous induction of melatonin increased the ACC content and ethylene production in grapevine and tobacco plants, respectively. The expression of <i>MYB108A</i> and <i>ACS1</i>, which function as a transcription factor and a key gene involved in ethylene production, respectively, was strongly induced by melatonin treatment. Additionally, MYB108A directly bound to the promoter of <i>ACS1</i> and activated its transcription. <i>MYB108A</i> expression promoted ACC synthesis and ethylene production by activating <i>ACS1</i> expression in response to melatonin treatment. The suppression of <i>MYB108A</i> expression partially limited the effect of melatonin on the induction of ethylene production and reduced melatonin-induced salt tolerance. Collectively, melatonin promotes ethylene biosynthesis and salt tolerance through the regulation of <i>ACS1</i> by MYB108A.