Abstract

Nitric oxide (NO), as a redox molecule, played important role in plant response to environmental stress. Here, we found that loss of tomato S-Nitrosoglutathione reductase ( SlGSNOR ), a critical regulator of NO balance, led to global sensitivity to heat, salt, bicarbonate, and paraquat stresses in tomato, suggesting that SlGSNOR was a positive regulator in tomato against abiotic stresses. In addition, under these stresses, loss of SlGSNOR induced excessive NO accumulation in the roots of the transgenic plant. Bicarbonate accumulation has been a limiting factor of tomato production in the north of China, and there were less reports on the regulation of bicarbonate stress compared with other abiotic stress, therefore, in the following experiment, the mechanism of SlGSNOR function focused on investigating bicarbonate tolerance. Proteomes data indicated that loss of SlGSNOR triggered the expression of proteins in MAPK and ethylene signaling pathway under bicarbonate condition. Importantly, loss of SlGSNOR increased ethylene emission under bicarbonate condition, meaning that ethylene signaling participated in SlGSNOR -mediated tomato bicarbonate stress tolerance. Interestingly, under bicarbonate stress, silencing SlMAPK3 or SlACO1 in SlGSNOR -RNAi tomato partially compromised the sensitivity and ethylene emission. Mechanistically, under bicarbonate stress, silencing SlMAPK3 in SlGSNOR -RNAi tomato plants suppressed the transcription of SlACO1 , whereas silencing SlACO1 in SlGSNOR -RNAi tomato activated the transcription of SlMAPK3 . Collectively, these data demonstrated that SlGSNOR -mediated tomato abiotic stress tolerance was depended on SlMAPK3 - SlACO1 cascade signaling, largely. In addition, the incorporation of global abiotic stress tolerance traits into crop plants may succeed by manipulating GSNOR expression. • Tomato GSNOR was a multiple stress-induced gene. • SlGSNOR was positively regulated tomato heat, salt, bicarbonate, and paraquat tolerance. • SlGSNOR -mediated bicarbonate tolerance was depended on SlMAPK3 - SlACO1 cascade signaling.

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