Beijing Advanced Innovation Center for Tree Breeding by Molecular Design, Beijing Forestry University, Beijing 10083, China; Umeå Plant Science Centre, Department of Forest Genetics and Plant Physiology, Swedish University of Agricultural Sciences, Umeå 901 87, Sweden.
Umeå Plant Science Centre, Department of Forest Genetics and Plant Physiology, Swedish University of Agricultural Sciences, Umeå 901 87, Sweden.
Curr Biol. 2020 May 4;30(9):1733-1739.e3. doi: 10.1016/j.cub.2020.02.055. Epub 2020 Mar 19.
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.
差异生长在形态发生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中，细胞扩展的局部差异导致器官水平的变形，如弯曲或弯曲[4,5]。在早期幼苗发育过程中，下胚轴的差异细胞伸长导致顶端弯钩结构的弯曲，从而保护茎尖分生组织免受从土壤中伸出时的损伤[6,7]。植物激素参与顶端弯钩的发育，但不参与它们如何机械地驱动差异生长[8]。在这里，我们通过将顶端弯钩发育作为实验模型，提供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。我们使用遗传和细胞生物学方法表明，木葡聚糖（一种主要的初生细胞壁成分）介导了表皮细胞不对称机械性能，这对于弯钩发育是必需的。木葡聚糖缺陷的 xxt1 xxt2 突变体[9]在差异细胞伸长和弯钩发育方面表现出严重缺陷。对 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，这对于建立生长素响应最大值对于弯钩内侧细胞伸长的优先抑制至关重要。遗传证据表明，生长素反应因子 ARF2 作为一个负调节剂，作用于木葡聚糖依赖性弯钩发育控制和极性生长素运输的转录控制的下游。我们的结果揭示了细胞壁和极性生长素运输的转录控制之间的关键反馈过程，这是植物中生长素依赖性差异细胞伸长控制的基础。
