Arabidopsis HAK5 under low K+ availability operates as PMF powered high-affinity K+ transporter
Tobias Maierhofer (),
Sönke Scherzer,
Armando Carpaneto (),
Thomas D. Müller,
Jose M. Pardo,
Inga Hänelt,
Dietmar Geiger and
Rainer Hedrich
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Tobias Maierhofer: Julius-Maximilians-Universität Würzburg
Sönke Scherzer: Julius-Maximilians-Universität Würzburg
Armando Carpaneto: University of Genova
Thomas D. Müller: Julius-Maximilians-Universität Würzburg
Jose M. Pardo: CSIC-Universidad de Sevilla
Inga Hänelt: Goethe University Frankfurt
Dietmar Geiger: Julius-Maximilians-Universität Würzburg
Rainer Hedrich: Julius-Maximilians-Universität Würzburg
Nature Communications, 2024, vol. 15, issue 1, 1-13
Abstract:
Abstract Plants can survive in soils of low micromolar potassium (K+) concentrations. Root K+ intake is accomplished by the K+ channel AKT1 and KUP/HAK/KT type high-affinity K+ transporters. Arabidopsis HAK5 mutants impaired in low K+ acquisition have been identified already more than two decades ago, the molecular mechanism, however, is still a matter of debate also because of lack of direct measurements of HAK5-mediated K+ currents. When we expressed AtHAK5 in Xenopus oocytes together with CBL1/CIPK23, no inward currents were elicited in sufficient K+ media. Under low K+ and inward-directed proton motive force (PMF), the inward K+ current increased indicating that HAK5 energetically couples the uphill transport of K+ to the downhill flux of H+. At extracellular K+ concentrations above 25 μM, the initial rise in current was followed by a concentration-graded inactivation. When we replaced Tyr450 in AtHAK5 to Ala the K+ affinity strongly decreased, indicating that AtHAK5 position Y450 holds a key for K+ sensing and transport. When the soil K+ concentration drops toward the range that thermodynamically cannot be covered by AKT1, the AtHAK5 K+/H+ symporter progressively takes over K+ nutrition. Therefore, optimizing K+ use efficiency of crops, HAK5 could be key for low K+ tolerant agriculture.
Date: 2024
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DOI: 10.1038/s41467-024-52963-6
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