Melatonin Coordinates Root Cell-Wall Zinc Remobilization and Shoot Transport via Nitric Oxide Signaling Under Zinc Deficiency in Rice.

Although zinc (Zn) deficiency severely inhibits rice growth, it remains unclear how melatonin (MT) promotes adaptation under conditions of insufficient Zn supply. To address this issue, rice seedlings were treated with MT, the NO donor sodium nitroprusside (SNP), or the NO scavenger c-PTIO, alone or in combination, under Zn-deficient conditions. Zn starvation rapidly promoted endogenous MT accumulation in rice roots, together with a 90.2%-179.5% rise in the transcript levels of MT biosynthetic genes. Exposure to Zn deprivation reduced root/shoot length and root/shoot biomass, by 46.2%/31.3% and 27.5%/39.6%, respectively. Among the tested concentrations, 10 μM MT produced the strongest protective effect, increasing root length, shoot height, root biomass, and shoot biomass by 59.9%, 34.2%, 21.7%, and 51.8%, respectively, relative to plants that were merely deficient in Zn. In Zn-deficient plants, MT raised Zn concentration in root and shoot both by 16.2% and xylem sap Zn concentration by 15.6%. MT also increased root cell-wall Zn content, pectin abundance, and pectin-associated Zn by 20.0%, 39.3%, and 31.9%, respectively. At the expression level, MT moderated the induction of OsZIP4, OsZIP5, OsZIP8, OsZIP9, OsZIP10, and OsHMA3 by Zn deficiency and further repressed OsZIP1, implying feedback regulation of the Zn-homeostasis network instead of direct activation of Zn-transporter transcription. Root NO content rose by 29.8% after MT treatment, and SNP elicited increases in root and shoot Zn concentrations comparable to those associated with MT. Overall, the data suggest that an NO-associated response contributes to MT-mediated Zn-deficiency tolerance by restoring Zn homeostasis, promoting apoplastic Zn remobilization and root-to-shoot transport, and limiting oxidative damage.