Differential growth plays a crucial role during morphogenesis [1-3]. In plants, development occurs within mechanically connected tissues, and local differences in cell expansion lead to deformations at the organ level, such as buckling or bending [4, 5]. During early seedling development, bending of hypocotyl by differential cell elongation results in apical hook structure that protects the shoot apical meristem from being damaged during emergence from the soil [6, 7]. Plant hormones participate in apical hook development, but not how they mechanistically drive differential growth [8]. Here, we present evidence of interplay between hormonal signals and cell wall in auxin-mediated differential cell elongation using apical hook development as an experimental model. Using genetic and cell biological approaches, we show that xyloglucan (a major primary cell wall component) mediates asymmetric mechanical properties of epidermal cells required for hook development. The xxt1 xxt2 mutant, deficient in xyloglucan [9], displays severe defects in differential cell elongation and hook development. Analysis of xxt1 xxt2 mutant reveals a link between cell wall and transcriptional control of auxin transporters PINFORMEDs (PINs) and AUX1 crucial for establishing the auxin response maxima required for preferential repression of elongation of the cells on the inner side of the hook. Genetic evidence identifies auxin response factor ARF2 as a negative regulator acting downstream of xyloglucan-dependent control of hook development and transcriptional control of polar auxin transport. Our results reveal a crucial feedback process between the cell wall and transcriptional control of polar auxin transport, underlying auxin-dependent control of differential cell elongation in plants.

中文翻译：

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细胞壁和生长素之间的相互作用介导顶端钩发育过程中差异细胞伸长的控制。

差异生长在形态发生过程中起着至关重要的作用 [1-3]。在植物中，发育发生在机械连接的组织内，细胞扩张的局部差异导致器官水平的变形，例如屈曲或弯曲 [4, 5]。在幼苗早期发育过程中，由于不同的细胞伸长导致下胚轴弯曲，从而形成顶端钩状结构，保护茎尖分生组织在从土壤中出苗时不被破坏 [6, 7]。植物激素参与顶端钩发育，但不参与它们如何机械地驱动差异生长 [8]。在这里，我们使用顶端钩发育作为实验模型，展示了激素信号和细胞壁在生长素介导的差异细胞伸长中相互作用的证据。使用遗传和细胞生物学方法，我们表明木葡聚糖（主要的主要细胞壁成分）介导钩子发育所需的表皮细胞的不对称机械特性。xxt1 xxt2 突变体缺乏木葡聚糖 [9]，在差异细胞伸长和钩状发育方面表现出严重缺陷。xxt1 xxt2 突变体的分析揭示了细胞壁与生长素转运蛋白 PINFORMEDs (PINs) 和 AUX1 的转录控制之间的联系，这对于建立优先抑制钩内侧细胞伸长所需的生长素反应最大值至关重要。遗传证据表明，生长素反应因子 ARF2 是一种负调节因子，在依赖木葡聚糖的钩子发育控制和生长素极性转运的转录控制下游起作用。