Leaf morphology is one of the most important features of the ideal plant architecture. However, the genetic and molecular mechanisms controlling this feature in crops remain largely unknown. Here, we characterized the rice (Oryza sativa) wide leaf 1 (wl1) mutant, which has wider leaves than the wild-type due to more vascular bundles and greater distance between small vascular bundles. WL1 encodes a Cys-2/His-2-type zinc finger protein that interacts with Tillering and Dwarf 1 (TAD1), a co-activator of the anaphase-promoting complex/cyclosome (APC/C) (a multi-subunit E3 ligase). The APC/CTAD1 complex degrades WL1 via the ubiquitin-26S proteasome degradation pathway. Loss-of-function of TAD1 resulted in plants with narrow leaves due to reduced vascular bundle numbers and distance between the small vascular bundles. Interestingly, we found that WL1 negatively regulated the expression of a narrow leaf gene, NARROW LEAF 1 (NAL1), by recruiting the co-repressor TOPLESS-RELATED PROTEIN and directly binding to the NAL1 regulatory region to inhibit its expression by reducing the chromatin histone acetylation. Furthermore, biochemical and genetic analyses revealed that TAD1, WL1, and NAL1 operated in a common pathway to control the leaf width. Our study establishes an important framework for understanding the APC/CTAD1-WL1-NAL1 pathway-mediated control of leaf width in rice, and provides insights for improving crop plant architecture.

中文翻译：

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APC/CTAD1-WIDE LEAF 1-NARROW LEAF 1 通路控制水稻的叶片宽度。

叶子形态是理想植物结构最重要的特征之一。然而，控制作物这一特征的遗传和分子机制仍然很大程度上未知。在这里，我们对水稻 (Oryza sativa) 宽叶 1 (wl1) 突变体进行了表征，该突变体由于维管束更多且小维管束之间的距离更大，因此比野生型具有更宽的叶子。WL1 编码 Cys-2/His-2 型锌指蛋白，可与分蘖和矮化 1 (TAD1) 相互作用，后者是后期促进复合物/环体 (APC/C)（多亚基 E3 连接酶）的共激活剂）。APC/CTAD1 复合物通过泛素-26S 蛋白酶体降解途径降解 WL1。由于维管束数量和小维管束之间的距离减少，TAD1 功能丧失导致植物叶片变窄。有趣的是，我们发现WL1通过招募共阻遏物TOPLESS-RELATED PROTEIN并直接与NAL1调节区结合，通过减少染色质组蛋白来抑制其表达，从而负向调节窄叶基因NARROW LEAF 1 (NAL1)的表达乙酰化。此外，生化和遗传分析表明，TAD1、WL1 和 NAL1 在控制叶宽的共同途径中发挥作用。我们的研究为理解 APC/CTAD1-WL1-NAL1 途径介导的水稻叶宽控制建立了一个重要框架，并为改善作物株型提供了见解。