A 48-bp deletion upstream of LIGULELESS 1 alters rice panicle architecture

Linhua Wu, Min Hu, Shuwei Lyu, Wenfeng Chen, Hang Yu, Qing Liu, Wei He, Chen Li, Zuofeng Zhu
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Abstract

Panicle architecture is an agronomic determinant of crop yield and a target for cereal crop improvement. To investigate its molecular mechanisms in rice, we performed map-based cloning and characterization of OPEN PANICLE 1 (OP1), a gain-of-function allele of LIGULELESS 1 (LG1), controlling the spread-panicle phenotype. This allele results from a 48-bp deletion in the LG1 upstream region and promotes pulvinus development at the base of the primary branch. Increased OP1 expression and altered panicle phenotype in pC1 chimeric transgenic plants and upstream-region knockout mutants indicated that the deletion regulates spread-panicle architecture in the mutant spread panicle 1 (sp1). Knockout BRASSINOSTEROID UPREGULATED1 (BU1) gene in the background of OP1 complementary plants showed compact panicles, suggesting OP1 may regulate inflorescence architecture via the brassinosteroid signaling pathway. We propose that manipulating the upstream regulatory region of OP1 or changing BR signal pathway could be an efficient way to improve rice inflorescence architecture.

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LIGULELESS 1 上游 48-bp 的缺失会改变水稻圆锥花序的结构
圆锥花序结构是作物产量的一个农艺决定因素,也是谷类作物改良的一个目标。为了研究水稻圆锥花序结构的分子机制,我们基于图谱克隆并鉴定了OPEN PANICLE 1(OP1),它是LIGULELESS 1(LG1)的一个功能增益等位基因,控制着圆锥花序的舒展表型。该等位基因源于 LG1 上游区域的 48-bp 缺失,可促进主枝基部的叶枕发育。pC1 嵌合转基因植株和上游区域基因敲除突变体中 OP1 表达的增加和圆锥花序表型的改变表明,该缺失调节了突变体平展圆锥花序 1(sp1)的平展圆锥花序结构。在 OP1 互补植株背景中敲除黄铜类固醇上调1(BU1)基因后,圆锥花序紧凑,表明 OP1 可能通过黄铜类固醇信号途径调控花序结构。我们认为,操纵 OP1 上游调控区或改变 BR 信号通路可能是改善水稻花序结构的有效方法。
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