The plant G-protein network, comprising G?, G?, and G? core subunits, regulates development, senses sugar, and mediates biotic and abiotic stress responses. Here in this paper, we report G-protein signalling in the salt stress response using two crop models, rice and maize. Loss-of-function mutations in the corresponding genes encoding the G? subunit attenuate growth inhibition and cellular senescence caused by sodium chloride (NaCl). G? null mutations conferred reduced leaf senescence, chlorophyll degradation, and cytoplasm electrolyte leakage under NaCl stress. Sodium accumulated in both wild-type and G?-mutant shoots to the same levels, suggesting that G? signalling controls cell death in leaves rather than sodium exclusion in roots. Growth inhibition is probably initiated by osmotic change around root cells, because KCl and MgSO<
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also suppressed seedling growth equally as well as NaCl. NaCl lowered rates of cell division and elongation in the wild-type leaf sheath to the level of the G?-null mutants
however there was no NaCl-induced decrease in cell division in the G? mutant, implying that the osmotic phase of salt stress suppresses cell proliferation through the inhibition of G?-coupled signalling. These results reveal two distinct functions of G? in NaCl stress in these grasses: attenuation of leaf senescence caused by sodium toxicity in leaves, and cell cycle regulation by osmotic/ionic stress.