lncRNA62732 acts as an eTM of miR9778 to regulate TaHAK18-5B and mediate the potassium deficiency response in wheat

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.