Melatonin suppression of heat-induced leaf senescence involves changes in abscisic acid and cytokinin biosynthesis and signaling pathways in perennial ryegrass (Lolium perenne L.)

Leaf senescence is a typical symptom of heat damage in cool-season plant species. The objective of this study was to determine whether melatonin could suppress heat-induced leaf senescence in perennial ryegrass (Lolium perenne L.) and whether melatonin interacted with abscisic acid (ABA) and cytokinin (CK) to exert its biological function. Perennial ryegrass (cv. ‘Pinnacle’) plants were foliar sprayed with melatonin or water and exposed to heat stress at 38/33 °C (day/night) and non-stress condition at 22/17 °C for 28 d in growth chambers. Exogenous application of melatonin alleviated growth inhibition and leaf senescence induced by heat stress, as manifested by significant higher tiller number, above-ground dry weight, plant height, turf quality, leaf chlorophyll (Chl) content, photochemical efficiency (Fv/Fm), net photosynthesis rate, and cell membrane stability in melatonin-treated plants compared to non-melatonin treatment under heat stress. The suppression of heat-induced leaf senescence by melatonin was also reflected by the reduction of transcript levels of senescence-associated genes (LpSAG12.1 and Lph36) in plants exposed to heat stress. Melatonin treatment increased the endogenous content of melatonin and CK content, whereas it decreased ABA content under heat stress. The expression of CK biosynthesis genes and its signaling response transcription factors (type B ARRs) were up-regulated, while the biosynthesis and signaling genes involved in ABA were down-regulated by melatonin treatment under heat stress. These results indicate that the suppression of heat-induced leaf senescence by exogenous melatonin could be associated with activating CK synthesis and signaling while inhibiting ABA synthesis and signaling in perennial ryegrass.