The study identifies specific lysine residues where the Arabidopsis transcription factor AtTCP8 is covalently modified by SUMO, showing that mutation of these sites abolishes sumoylation and impairs the protein's ability to rescue a tcp8 brassinosteroid signaling defect and activate target promoters. Parallel experiments reveal that class I TCP orthologs in the moss Physcomitrium patens are also sumoylated, suggesting a conserved post‑translational regulatory mechanism across vascular and non‑vascular plants.