提出问题：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.

主要研究：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. 

结果1-必要性：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.

结果2-下游基因：These two pathways act synergistically to downregulate the expression of BRC1, a conserved inhibitor of shoot branching.

结果3-转录抑制BRC1：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. 

结果4-不同机制：Glycolysis/TCA-cycle- and OPPP-dependent regulations involve the -1973bp/-1611bp and -1206bp/-709bp regions of pRhBRC1, respectively.

综上：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.

分枝是植物生长和发育的一个重要进程，由生长素和糖拮抗调控。激素对于分枝的调控机制已经研究的比较深入了，但是糖信号在芽向外生长过程中的作用还有待进一步研究。基于一个逐步和全面策略，作者研究了糖酵解/三羧酸（TCA）循环和氧化戊糖磷酸途径（OPPP）在控制芽向外生长中的作用。作者发现这两个通路是植物断顶和响应糖可利用性时，芽向外生长的必要条件。同时，这两个通路也是生长素和糖可利用性拮抗调控交互作用的靶标。这两个通路协同工作，下调茎分枝抑制因子BRC1基因的表达。利用RhBRC1基因的启动子pRhBRC1融合GFP蛋白，稳定转化蔷薇愈伤组织，发现糖酵解/TCA循环和OPPP协同抑制pRhBRC1的转录活性。糖酵解/TCA循环和OPPP依赖性的调控分别涉及RhBRC1启动子的-1973bp/-1611bp和-1206bp/-709bp区域序列。综上，本文的研究揭示了糖酵解/三羧酸循环和OPPP途径参与植物茎分枝的调控，很有可能通过不同的分子机制将植物的内源因子和芽向外生长的发育进程关联到一起。