背景回顾：The control of apical dominance involves auxin, strigolactones (SLs), cytokinins (CKs), and sugars, but the mechanistic controls of this regulatory network are not fully understood. 

主要发现：Here, we show that brassinosteroid (BR) promotes bud outgrowth in tomato through the direct transcriptional regulation of BRANCHED1(BRC1) by the BR signaling component BRASSINAZOLE-RESISTANT1 (BZR1). 

结果1-各种处理下的芽向外生长响应：Attenuated responses to the removal of the apical bud, the inhibition of auxin, SLs or gibberellin synthesis, or treatment with CK and sucrose, were observed in bud outgrowth and the levels of BRC1 transcripts in the BR-deficient or bzr1 mutants. 

结果2-各种处理下的BR积累：Furthermore, the accumulation of BR and the dephosphorylated form of BZR1 were increased by apical bud removal, inhibition of auxin, and SLs synthesis or treatment with CK and sucrose. 

结果3-DELLA缺陷突变体：These responses were decreased in the DELLA-deficient mutant.

结果4-CK积累：In addition, CK accumulation was inhibited by auxin and SLs, and decreased in the DELLA-deficient mutant, but it was increased in response to sucrose treatment. 

结果5-CK促进BR合成：CK promoted BR synthesis in axillary buds through the action of the type-B response regulator, RR10. 

结论：Our results demonstrate that BR signaling integrates multiple pathways that control shoot branching. Local BR signaling in axillary buds is therefore a potential target for shaping plant architecture.

 摘 要 

顶端优势的控制涉及到生长素、独脚金内酯（SLs）、细胞分裂素（CK）和糖，但控制这种调控网络的机制还不完全清楚。本文中，作者发现番茄中油菜素内酯（BR）通过BR信号转导组分BZR1直接转录调控BRC1，从而促进芽向外生长。对BR缺陷或bzr1突变体进行去除顶芽、抑制生长素、SLs或者赤霉素的合成、亦或是用细胞分裂素和蔗糖处理，芽向外生长和BRC1转录水平的响应减弱。此外，去除顶芽、抑制生长素和SLs的合成，或者用CK和蔗糖处理，发现BR的积累和BZR1的去磷酸化增加。在DELLA缺陷突变株里，这些响应均减弱。另外，生长素和SLs均能够抑制CK的积累，并且在DELLA缺陷突变株中CK含量减少，但是蔗糖处理时CK含量增加。CK通过type-B响应调控子RR10的作用促进腋芽中BR的合成。本文的结果揭示了BR信号转导整合了多个途径，控制茎分枝。因此，腋芽区域的BR信号转导是塑造植物结构的潜在靶标。