Wounding-Induced Redirection of Sugar Transport Fuels Tissue Repair

Wounding triggers growth programs to restore damaged tissues, creating a local surge in metabolic demand. How resource recruitment is modified to meet this demand is unclear. Here, we show that regeneration of dissected root tips is dependent on photosynthetic sucrose in a dose-dependent manner, although sucrose itself is excluded from the injury site. High-resolution tracking of Glifon, a novel live glucose reporter, reveals that glucose accumulates near the cut. Glucose accumulation required the apoplasmic sugar transport components CELL WALL INVERTASE (CWINV) and SUGAR TRANSPORTER PROTEINS (STP), which were rapidly induced by wounding. Loss of CWINV or STP function compromised root repair, particularly under limited sucrose availability, whereas increased STP13 gene dosage enhanced repair rates. Similar sugar transport genes were activated in other wounding contexts and promoted wound-induced adventitious root initiation. We propose that injury elicits a proactive local shift in sugar flow to promote resource recruitment and sustain tissue repair. Significance StatementPlants grow under constant physical assault and have evolved mechanisms to repair damaged organs. Wound repair increases demand for sugars to fuel cell division and growth, but unlike animals, plants cannot dilate blood vessels and rely on fixed phloem tubes. Our work shows how plants solve this problem. We uncover a circuit that blocks entry of the transported sugar sucrose into the wound site, converting it to glucose in the cell wall space, which is then rapidly imported into injury-adjacent cells. This wound-induced mechanism precedes repair, creating a proactive "sugar sink" that draws carbohydrates toward the damaged zone. Boosting this mechanism increases wound repair rates, suggesting this mechanism allows plants to control resource distribution, balancing growth and wound repair.