Overexpression of OsHAK5 potassium transporter enhances virus resistance in rice (Oryza sativa)

Intracellular potassium (K+) transported by plants under the action of a number of transport proteins is crucial for plant survival under distinct abiotic and biotic stresses. A correlation between K+ status and disease incidence has been found in many studies, but the roles of K+ in regulating disease resistance to viral diseases remain elusive. Here, we report that HIGH-AFFINITY K+ TRANSPORTER 5 (OsHAK5) regulates the infection of rice grassy stunt virus (RGSV), a negative-sense single-stranded bunyavirus, in rice (Oryza sativa). We found the K+ content in rice plants was significantly inhibited on RGSV infection. Meanwhile, a dramatic induction of OsHAK5 transcripts was observed in RGSV-infected rice plants and in rice plants with K+ deficiency. Genetic analysis indicated that disruption of OsHAK5 facilitated viral pathogenicity. In contrast, overexpression of OsHAK5 enhanced resistance to RGSV infection. Our analysis of reactive oxygen species (ROS) including H2O2 and O2-, by DAB and NBT staining, respectively, indicated that RGSV infection as well as OsHAK5 overexpression increased ROS accumulation in rice leaves. The accumulation of ROS is perhaps involved in the induction of host resistance against RGSV infection in OsHAK5 transgenic overexpression rice plants. Furthermore, RGSV-encoded P3 induced OsHAK5 promoter activity, suggesting that RGSV P3 is probably an elicitor for the induction of OsHAK5 transcripts during RGSV infection. These findings indicate the crucial role of OsHAK5 in host resistance to virus infection. Our results may be exploited in the future to increase crop yield as well as improve host resistance via genetic manipulations.

Automated summary

Intracellular potassium (K+) is essential for plant survival under different stresses. This study reveals the role of the OsHAK5 protein in regulating rice resistance to the viral disease RGSV. The overexpression of OsHAK5 enhances resistance to RGSV infection by increasing reactive oxygen species (ROS) accumulation. The findings suggest the crucial role of OsHAK5 in host resistance to virus infection.