The NADPH oxidase OsRbohA increases salt tolerance by modulating K+ homeostasis in rice

Rice (Oryza sativa L.) is a staple cereal for more than two thirds of the world's population. Soil salinity severely limits rice growth, development, and grain yield. It is desirable to elucidate the mechanism of rice's salt-stress response. As the major source of H2O2, NADPH oxidase (Rboh) is believed to be involved in salt-stress tolerance. However, the function and mechanism of rice Rboh in salt stress response remain unclear. In this study, we found that the expression of OsRbohA was up-regulated by NaCl treatment in the shoots and roots of rice seedlings. Knockout of OsRbohA reduced the tolerance of rice to salt stress. Knockout of OsRbohA blocked NaCl-induced increases of NADPH activity and H2O2 content in roots. OsRbohA knockout inhibited root growth and disrupted K+ homeostasis by reducing the expression of K+ transporters and channel-associated genes (OsGORK, OsAKT1, OsHAK1, and OsHAK5) in roots under NaCl treatment. Under NaCl treatment, OsRbohA knockout also reduced subcellular K+ contents of the plasma membrane and soluble fraction. Overexpression of OsRbohA increased the expression of K+ transporters and channel-associated genes and reduced the loss of K+ ions in roots. These results indicate that OsRbohA-mediated H2O2 accumulation modulates K+ homeostasis, thereby increasing salt tolerance in rice.