The miR1118-TaCaM5-3A Module Regulates K+ Uptake and Enhances K+ Deficiency Tolerance in Wheat (Triticum aestivum L.).

Abstract

Potassium (K+) deficiency significantly decreases the productivity of crops (e.g., wheat). MicroRNAs (miRNAs) are master regulators of plant responses to stress, including K+ deficiency. In our previous study, miR1118 was identified as a Triticeae-specific miRNA that is highly expressed at multiple time points after exposure to K+ deficiency; however, the regulatory roles of miR1118 and its target gene TaCaM5-3A (calmodulin-encoding gene) in K+ uptake and tolerance to K+ deficiency remained unclear. In this study, miR1118 enhances the tolerance of wheat to K+ deficiency by improving K+ uptake capacity under K+ deficiency conditions, and simultaneously increases grain yield. TaCaM5-3A, as a target of miR1118, negatively regulates K+ uptake and decreased wheat tolerance to K+ deficiency. Additional analyses revealed that TaCaM5-3A physically interacts with TaHAK1-2A at the key residue I172 via a calcium (Ca2+)-independent pathway, which not only downregulates TaHAK1-2A protein levels but also decreases its apparent affinity for K+-binding. Collectively, the miR1118-TaCaM5-3A functional module modulates plant K+ uptake capacity by influencing the protein level and the K+ uptake activity of TaHAK1-2A, thereby playing a critical role in determining wheat tolerance to K+ deficiency and providing valuable information for breeding wheat varieties with high potassium efficiency.