LcHXK1 mediates glucose signaling to inhibit fruit abscission by phosphorylating LcWRKY42, a feedback regulator in...

Organ abscission is a core developmental process that allows plants to optimize resource allocation, maximize reproductive fitness, and respond to environmental cues. In agricultural systems, however, premature fruit abscission can severely reduce yield. Here, we investigate premature fruit drop in litchi and identify the hexokinase homolog LcHXK1 as a nonglycolytic hexose sensor that suppresses abscission by activating a pedicel lignification program. LcHXK1 physically associates with and phosphorylates the WRKY transcription factor LcWRKY42, a modification that enhances its stability and transcriptional activity in inducing laccase and peroxidase genes required for lignin polymerization, promoting lignin deposition and reinforcing the pedicel to prevent organ detachment. Over expression of LcHXK1 or LcWRKY42 in litchi callus and in Arabidopsis elevates lignin content, increases laccase and peroxidase activities, and delays organ abscission, revealing a conserved sugar-responsive pathway. LcWRKY42 also upregulates LcHXK1, forming a positive feedback loop that amplifies hexose signaling. Together, these findings define a sugar-sensing regulatory module that couples carbon status to pedicel lignification, providing a mechanistic framework for improving fruit retention in crops.