Potassium transporter OsHAK18 mediates potassium and sodium circulation and sugar translocation in rice.

High-affinity potassium (K+) transporter (HAK)/K+ uptake permease (KUP)/K+ transporter (KT) have been identified in all genome-sequenced terrestrial plants. They play an important role in K+ acquisition and translocation and in enhancing salt tolerance. Here, we report that plasma membrane-located OsHAK18 functions in K+ and sodium (Na+) circulation and sugar translocation in rice (Oryza sativa). OsHAK18 was expressed mainly, though not exclusively, in vascular tissues and particularly in the phloem. Knockout (KO) of OsHAK18 reduced K+ concentration in phloem sap and roots but increased K+ accumulation in the shoot of both 'Nipponbare' and 'Zhonghua11' cultivars, while overexpression (OX) of OsHAK18 driven by its endogenous promoter increased K+ concentration in phloem sap and roots and promoted Na+ retrieval from the shoot to the root under salt stress. Split-root experimental analysis of rubidium (Rb+) uptake and circulation indicated that OsHAK18-OX promoted Rb+ translocation from the shoot to the root. In addition, OsHAK18-KO increased while OsHAK18-OX reduced soluble sugar content in the shoot and oppositely affected the sugar concentration in the phloem and its content in the root. Moreover, OsHAK18-OX dramatically increased grain yield and physiological K+ utilization efficiency. Our results suggest that-unlike other OsHAKs analyzed heretofore-OsHAK18 is critical for K+ and Na+ recirculation from the shoot to the root and enhances the source-to-sink translocation of photo-assimilates.

The Potassium Transporter OsHAK5 Alters Rice Architecture via ATP-Dependent Transmembrane Auxin Fluxes.

Plant HAK/KUP/KT family members function as plasma membrane (PM) H+/K+ symporters and may modulate chemiosmotically-driven polar auxin transport (PAT). Here, we show that inactivation of OsHAK5, a rice K+ transporter gene, decreased rootward and shootward PAT, tiller number, and the length of both lateral roots and root hairs, while OsHAK5 overexpression increased PAT, tiller number, and root hair length, irrespective of the K+ supply. Inhibitors of ATP-binding-cassette type-B transporters, NPA and BUM, abolished the OsHAK5-overexpression effect on PAT. The mechanistic basis of these changes included the OsHAK5-mediated decrease of transmembrane potential (depolarization), increase of extracellular pH, and increase of PM-ATPase activity. These findings highlight the dual roles of OsHAK5 in altering cellular chemiosmotic gradients (generated continuously by PM H+-ATPase) and regulating ATP-dependent auxin transport. Both functions may underlie the prominent effect of OsHAK5 on rice architecture, which may be exploited in the future to increase crop yield via genetic manipulations.