The Pivotal Involvement of the Respiratory burst oxidase G (SlRbohG) Gene in H2O2 Production Under Stress for Proper Na+ Homeostasis Regulation in Tomato

Abstract

Regulation of sodium homeostasis is crucial for plant response to salinity conditions. Here we report on the genetic and physiological characterization of two tomato allelic mutants, sodium gatherer1-2 (sga1-2), which exhibit pronounced chlorosis and hyperhydration under salt stress. Mapping-by-sequencing revealed that mutant phenotype resulted from mutations in the SlRbohG gene, and CRISPR/Cas9 knockouts of this gene gave phenocopies of the sga1-2 mutants. Physiological analyses showed that sga1-2 salt hypersensitivity is linked to an increase of Na+ and water transport from roots to shoots, which explains their extreme chlorosis and hyperhydration under salinity conditions. At the molecular level, SlPIP2;12 gene, an aquaporin down-regulated in the WT under salt stress, was overexpressed in the sga1-2 mutants, which could enhance water transport to the shoot. Also, sga1-2 mutants exhibited a significant reduction in the expression of key sodium transporters, thus modifying the normal distribution of Na+ in tomato plant tissues. Furthermore, treatment of WT plants with the NADPH oxidase inhibitor DPI prevented H2O2 production in response to salinity, resulting in elevated Na+ accumulation in the shoot and reduced expression of the SlHKT1;2 gene in root. Altogether, our results show that SlRbohG plays a central role in salt tolerance through ROS-mediated signaling. HIGHLIGHTLoss of function of tomato SlRbohG gene leads hypersensibility to salt stress due to increased Na+ and water transport from root to shoot.