Bud outgrowth is controlled by environmental and endogenous factors. Through the use of the photosynthesis inhibitor, norflurazon, and of masking experiments, evidence is given here that light acts mainly as a morphogenic signal in the triggering of bud outgrowth, and that initial steps in the light signaling pathway involve cytokinins (CK). Indeed, in rose, inhibition of bud outgrowth by darkness is suppressed solely by application of CK. In contrast, application of sugars has limited effect. Exposure of plants to white light (WL) induces a rapid (after 3 to 6h WL exposure) up-regulation of CK synthesis (RhIPT3, RhIPT5), of CK activation (RhLOG8) and of CK putative transporter RhPUP5 genes and to the repression of the CK degradation RhCKX1 gene in the node. This leads to accumulation of CK in the node within 6h and in the bud at 24h and to the triggering of bud outgrowth. Molecular analysis of genes involved in major mechanisms of bud outgrowth (strigolactones signaling (RwMAX2), metabolism and transport of auxin (RhPIN1, RhYUC1, RhTAR1), regulation of sugars sink strength (RhVI, RhSUSY, RhSUC2, RhSWEET10), cell division and expansion (RhEXP, RhPCNA)) reveal that when supplied in darkness, CK up-regulate their expression as rapidly and as intensely as WL. Additionally, up-regulation of CK by WL promotes xylem flux towards the bud as evidenced by methylene blue accumulation in the bud after CK treatment in the dark. Altogether, these results suggest that CK are initial components of the light-signaling pathway that controls initiation of bud outgrowth.