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

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.