<scp>lncRNA62732</scp> acts as an <scp>eTM</scp> of <scp>miR9778</scp> to regulate <scp>TaHAK18</scp> ‐ <scp>5B</scp> and mediate the potassium deficiency response in wheat

Summary Potassium (K + ) deficiency severely limits global wheat productivity and food security. Genetic improvement of K + utilization efficiency (KUE) is a sustainable strategy to address this challenge; however, the underlying molecular mechanisms remain unclear. We identified a lncRNA62732‐miR9778‐ TaHAK18‐5B module in wheat ( Triticum aestivum ) using long noncoding RNAs (lncRNA)‐sequencing combined with competing endogenous RNA prediction. Using genetic transformation and molecular biology techniques, we analyzed the role of this module in mediating the response to K + deficiency and the mechanisms underlying its effects. miR9778 is a Triticeae‐specific miRNA that directly targets TaHAK18‐5B. Both miR9778 silencing and TaHAK18‐5B overexpression notably enhanced K + deficiency tolerance at the seedling stage by modulating root K + acquisition and translocation from the roots to the shoots, whereas silencing TaHAK18‐5B had the opposite effect. Additionally, lncRNA62732 was identified as an endogenous target mimic (eTM) of miR9778 that sequesters miR9778 and prevents miR9778‐mediated cleavage of TaHAK18‐5B , thereby positively regulating wheat seedlings' growth under K + deficiency conditions. Notably, the lncRNA62732‐miR9778‐ TaHAK18‐5B module improved wheat adaptation to K + deficiency and enhanced the KUE and grain yield under field conditions. These results reveal a novel module in mediating K + homeostasis and provide valuable genetic resources for engineering KUE in wheat.