Shoot branching, determining plant architecture and crop yield, is critically controlled by strigolactones (SLs). However, how SLs inhibit shoot branching after its perception by the receptor complex remains largely obscure. In this study, using the transcriptomic and genetic analyss as well as biochemical studies, we reveal the key role of BES1 in the SL-regulated shoot branching. We demonstrate that BES1 and D53-like SMXLs, the substrates of SL receptor complex D14–MAX2, interact with each other to inhibit BRC1 expression, which specifically triggers the SL-regulated transcriptional network in shoot branching. BES1 directly binds the BRC1 promoter and recruits SMXLs to inhibit BRC1 expression. Interestingly, despite being the shared component by SL and brassinosteroid (BR) signaling, BES1 gains signal specificity through different mechanisms in response to BR and SL signals.

枝条分枝，决定植物结构和作物产量，受到独脚金内酯 (SL) 的严格控制。然而，在被受体复合物感知后，SLs 如何抑制枝条分枝在很大程度上仍然是模糊的。在这项研究中，使用转录组学和遗传分析以及生化研究，我们揭示了 BES1 在 SL 调节的枝条分枝中的关键作用。我们证明 BES1 和 D53 样 SMXLs，SL 受体复合物 D14-MAX2 的底物，相互相互作用以抑制BRC1表达，这在枝条分支中特异性触发 SL 调节的转录网络。BES1 直接结合BRC1启动子并招募 SMXL 来抑制BRC1表达。有趣的是，尽管 BES1 是 SL 和油菜素类固醇 (BR) 信号的共享成分，但 BES1 通过响应 BR 和 SL 信号的不同机制获得了信号特异性。