The circadian clock protein CmLHY integrates strigolactone signaling to regulate short-day-induced flowering in chrysanthemum

Yi Zhang, Yingying Xing, Xinhui Wang, Fei Li, Guosheng Xiong, Tao Huang, Yonggang Liu, Lisheng Zhai, Ting Zhang, Jiafu Jiang, Likai Wang, Fadi Chen, Sumei Chen
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Abstract

Flowering is a key ornamental trait in chrysanthemum and a major agronomic trait affecting rice yield. Strigolactones (SLs) are a class of phytohormones that regulate diverse aspects of plant growth and development, including flowering time. However, the molecular mechanisms underlying SL-mediated regulation of flowering remain poorly understood. Here, we show that SL promotes flowering in chrysanthemum under inductive short-day conditions. The SL-specific signaling complex CmMAX2–CmD14.1–CmD53 was first identified in chrysanthemum. Silencing CmD14.1 or CmMAX2 causes late-flowering and SL insensitivity, while their overexpression accelerates flowering upon SL treatment. In contrast, overexpression of CmD53 or the degradation-resistant variant CmD53m delayed flowering. SL-induced CmD53 degradation depends on both CmD14.1 and CmMAX2. RNA-seq analysis reveals that overexpression of CmD53 or CmD53m significantly downregulates the florigen gene CmFTL3. We confirmed that CmD53 directly binds to the CmFTL3 promoter to repress its transcription, thereby delaying flowering. Moreover, the central circadian clock protein CmLHY represses CmMAX2 and CmD14.1 transcription and subsequently modulates SL-mediated CmD53 degradation. This regulatory cascade fine-tunes CmFTL3 expression and controls flowering in chrysanthemum under inductive SD conditions. Similarly, in rice, OsD3 (a MAX2 homolog) and OsD14 act downstream of OsCCA1 (an LHY/CCA1 homolog) to regulate flowering. Our findings demonstrate that LHY/CCA1-mediated integration of SL signaling in the flowering regulatory pathway is conserved between chrysanthemum and rice, providing new insights into the novel crosstalk between the circadian clock and SL signaling in flowering-time control.
生物钟蛋白CmLHY整合了独角麦内酯信号,调节菊花短日诱导的开花
开花是菊花重要的观赏性状,也是影响水稻产量的主要农艺性状。独角金内酯(SLs)是一类植物激素,调节植物生长发育的各个方面,包括开花时间。然而,sl介导的开花调控的分子机制仍然知之甚少。本研究表明,SL在诱导短日照条件下促进菊花开花。sl特异性信号复合物CmMAX2-CmD14.1-CmD53首次在菊花中被鉴定。沉默CmD14.1或CmMAX2会导致延迟开花和SL不敏感,而它们的过表达会加速SL处理后的开花。相比之下,过表达CmD53或抗降解变体CmD53m会延迟开花。sl诱导的CmD53降解依赖于CmD14.1和CmMAX2。RNA-seq分析显示,过表达CmD53或CmD53m可显著下调成花基因CmFTL3。我们证实CmD53直接结合CmFTL3启动子抑制其转录,从而延迟开花。此外,中央生物钟蛋白CmLHY抑制CmMAX2和CmD14.1的转录,随后调节sl介导的CmD53降解。这个调控级联调控CmFTL3的表达并控制菊花在诱导SD条件下的开花。同样,在水稻中,OsD3(一个MAX2同源物)和OsD14在OsCCA1(一个LHY/CCA1同源物)的下游作用来调节开花。我们的研究结果表明,LHY/ cca1介导的SL信号在开花调控途径中的整合在菊花和水稻之间是保守的,这为生物钟和SL信号在开花时间控制中的新型串音提供了新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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