Axillary bud outgrowth in rose is controlled by sugar metabolic and signalling pathways

Shoot branching is a pivotal process during plant growth and development, antagonistically orchestrated by auxin and sugars. By contrast to extensive investigations on hormonal regulatory networks, our current knowledge on the role of sugar signalling pathways in bud outgrowth is still scarce. Based on a stepwise and comprehensive strategy, we investigated the role of glycolysis/the tricarboxylic acid (TCA) cycle and the oxidative pentose phosphate pathway (OPPP) in the control of bud outgrowth. We demonstrated that these two pathways are necessary for bud outgrowth promotion upon plant decapitation and in response to sugar availability. They are also targets of the antagonistic crosstalk between auxin and sugar availability. These two pathways act synergistically to downregulate the expression of BRC1, a conserved inhibitor of shoot branching. Using Rosa calluses stably transformed with GFP-fused promoter sequences of RhBRC1 (pRhBRC1), glycolysis/TCA-cycle and the OPPP were found to repress the transcriptional activity of pRhBRC1 cooperatively. Glycolysis/TCA-cycle- and OPPP-dependent regulations involve the -1973bp/-1611bp and -1206bp/-709bp regions of pRhBRC1, respectively. Taken together, our findings indicate that glycolysis/the tricarboxylic acid cycle and the OPPP are integrative parts of shoot branching control and can link endogenous factors to the developmental program of bud outgrowth, more likely through two distinct mechanisms.