• Shoot branching is regulated by multiple signals. Previous studies have indicated that sucrose may promote shoot branching through suppressing the inhibitory effect of the hormone strigolactone (SL). However, the molecular mechanisms underlying this effect are unknown.
• Here, we used molecular and genetic tools to identify the molecular targets underlying the antagonistic interaction between sucrose and SL.
• We showed that sucrose antagonizes the suppressive action of SL on tillering in rice and on the degradation of D53, a major target of SL signalling. Sucrose inhibits the gene expression of D3, the orthologue of the Arabidopsis F-box MAX2 required for SL signalling. Overexpression of D3 antagonizes sucrose inhibition of D53 degradation and enables the SL inhibition of tillering under high sucrose. Sucrose prevents SL-induced degradation of D14, the SL receptor involved in D53 degradation. In contrast to D3, D14 overexpression enhances D53 protein levels and sucrose-induced tillering, even in the presence of SL.
• Our results show that sucrose inhibits SL response by affecting key components of SL signalling and, together with previous studies reporting the inhibition of SL synthesis by nitrate and phosphate, demonstrate the central role played by SLs in the regulation of plant architecture by nutrients.

中文翻译：

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蔗糖促进水稻 D53 积累和分蘖

• 枝条分枝受多种信号调控。先前的研究表明，蔗糖可能通过抑制激素独脚金内酯（SL）的抑制作用来促进枝条分枝。然而，这种效应背后的分子机制尚不清楚。
• 在这里，我们使用分子和遗传工具来确定蔗糖和 SL 之间拮抗相互作用的分子靶点。
• 我们发现蔗糖拮抗 SL 对水稻分蘖和 D53 降解的抑制作用，D53 是 SL 信号传导的主要目标。蔗糖抑制 D3 的基因表达，D3是 SL 信号传导所需的拟南芥 F-box MAX2的直系同源物。D3的过表达拮抗蔗糖对 D53 降解的抑制作用，并能够在高蔗糖条件下抑制分蘖的 SL。蔗糖可防止 SL 诱导的 D14 降解，D14 是参与 D53 降解的 SL 受体。与D3相比，D14过表达增强了 D53 蛋白水平和蔗糖诱导的分蘖，即使在 SL 存在下也是如此。
• 我们的研究结果表明，蔗糖通过影响 SL 信号传导的关键成分来抑制 SL 反应，并且与先前报告的硝酸盐和磷酸盐抑制 SL 合成的研究一起，证明了 SL 在营养物质调节植物结构中所起的核心作用。