Brassinosteroid signaling integrates multiple pathways to release apical dominance in tomato.
Brassinosteroid signaling integrates multiple pathways to release apical dominance in tomato.
复制标题
油菜素类固醇信号传导整合多种途径以释放番茄的顶端优势
DOI：
10.1073/pnas.2004384118
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发表时间：
2021-03-16
影响因子：
11.1
通讯作者：
Yu J
中科院分区：
文献类型：
--
作者：
Xia X;Dong H;Yin Y;Song X;Gu X;Sang K;Zhou J;Shi K;Zhou Y;Foyer CH;Yu J
近世纪来，生长素一直被认为是顶端优势的主要调节因子。然而，最近，糖被证明是顶端优势的初始调节剂，而独脚金内酯（SL）和细胞分裂素（CK）的下游生长素控制芽的生长。然而，不同途径的相互作用仍然是悬而未决的问题。在这里，我们报告说，油菜素类固醇（BR）是至关重要的释放顶端优势在番茄。CK信号传递来自生长素、SL和糖的信息以促进BR的产生，BR激活BZR 1转录因子以抑制BRANCHED 1的表达，BRANCHED 1是芽生长的抑制剂。这些研究结果表明，激素和代谢途径影响一个共同的BR信号控制拍摄分支。顶端优势的控制涉及生长素，独脚金内酯（SL），细胞分裂素（CK），和糖，但这种调节网络的机制控制还没有完全理解。在这里，我们表明，油菜素类固醇（BR）促进芽生长在番茄通过直接转录调控BRANCHED 1（BRC 1）的BR信号成分BRASSINAZOLE-RESISTANT 1（BZR 1）。减弱反应，以消除顶芽，生长素，SL或赤霉素合成的抑制，或用CK和蔗糖处理，观察芽生长和BRC 1转录水平的BR-缺陷或bzr 1突变体。此外，BR和BZR 1的去磷酸化形式的积累增加顶芽去除，抑制生长素，SL合成或处理与CK和蔗糖。这些反应在DELLA缺陷突变体中降低。此外，生长素和SL抑制CK积累，并在DELLA缺陷型突变体中减少，但它响应于蔗糖处理增加。CK通过B型反应调节因子RR 10的作用促进腋芽BR的合成。我们的研究结果表明，BR信号集成了多个途径，控制拍摄分支。因此，腋芽中的局部BR信号传导是塑造植物结构的潜在靶标。
For almost a century, auxin had been well-known as the master regulator of apical dominance. Recently, however, sugars were shown to be the initial regulator of apical dominance, while strigolactones (SLs) and cytokinins (CKs) act downstream of auxin to control bud outgrowth. However, the interactions of the different pathways have remained outstanding questions. Here, we report that brassinosteroids (BRs) are essential for the release of apical dominance in tomato. CK signaling relays information from auxin, SL, and sugars to promote the production of BRs, which activate the BZR1 transcription factor to suppress the expression of BRANCHED1, an inhibitor of bud outgrowth. These findings demonstrate that hormonal and metabolic pathways impinge on a common BR signaling for controlling shoot branching. 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. 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). 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. 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. These responses were decreased in the DELLA-deficient mutant. 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. CK promoted BR synthesis in axillary buds through the action of the type-B response regulator, RR10. 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.
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影响因子：
13.8
作者：
Divi, Uday K.;Rahman, Tawhidur;Krishna, Priti
通讯作者：
Krishna, Priti
影响因子：
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作者：
Kebrom, Tesfamichael H.;Chandler, Peter M.;Spielmeyer, Wolfgang
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Schaller, G. Eric
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