Melatonin confers saline-alkali tolerance by relieving nitrosative damage and S-nitrosylation of plasma membrane H+-ATPase 2 in tomato

ABSTRACT: Soil salination and alkalization are global problems impairing plant survival by disrupting REDOX homeostasis. Whether melatonin regulates REDOX homeostasis at nitrosative level, and thus affects plant saline-alkali tolerance remains unknown. In saline-alkali stress, excess nitric oxide (NO) causes nitrosative damage in tomato roots. This NO can be degraded by S-nitrosoglutathione reductase (GSNOR), or stimulates caffeic acid O-methyltransferase (COMT) transcript for melatonin synthesis. Melatonin further feedback scavenges excess NO to alleviate nitrosative damage at the whole protein level, indicating by proteome S-nitrosylation. We target plasma membrane H+-ATPase 2 (HA2) and highlight that HA2 is S-nitrosylated at Cys206 in saline-alkali stress, reducing HA activity, H+ efflux, and tolerance by impairing its interaction with 14-3-3 protein 1 (TFT1). In agreement with these observations, COMT-mediated melatonin relieves the HA2 S-nitrosylation to recover its function and saline-alkali tolerance. Therefore, we propose NO and melatonin as a pair of REDOX switches to control HA2 S-nitrosylation and saline-alkali tolerance. Under natural saline-alkali conditions, tomato productivity can be improved by grafting with COMT-, GSNOR-, HA2-overexpression rootstocks or by genetic engineering non-nitrosylated HA2C206S mutants. Using melatonin-NO-HA2 module as a case, this study illuminates a novel molecular function of melatonin and relevant genetic engineering strategies in future agriculture.

INSTRUMENT(S):

ORGANISM(S): 'solanum Lycopersicum' Phytoplasma

TISSUE(S): Root

SUBMITTER: guochen qin  

LAB HEAD: guochen qin

PROVIDER: PXD056815 | Pride | 2025-04-28

REPOSITORIES: Pride