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氯化镉通过扰乱肌动蛋白丝和钙离子梯度,抑制囊泡运输,从而改变拟南芥根毛细胞壁的构建。

Disarrangement of actin filaments and Ca²⁺ gradient by CdCl₂ alters cell wall construction in Arabidopsis thaliana root hairs by inhibiting vesicular trafficking.

机构信息

Key Laboratory of Photosynthesis and Molecular Environmental Physiology, Institute of Botany, Chinese Academy of Sciences, Xiangshan, Beijing 100093, China.

出版信息

J Plant Physiol. 2011 Jul 15;168(11):1157-67. doi: 10.1016/j.jplph.2011.01.031. Epub 2011 Apr 15.

Abstract

Cadmium (Cd), one of the most toxic heavy metals, inhibits many cellular and physiological processes in plants. Here, the involvement of cytoplasmic Ca²⁺ gradient and actin filaments (AFs) in vesicular trafficking, cell wall deposition and tip growth was investigated during root (hair) development of Arabidopsis thaliana in response to CdCl₂ treatment. Seed germination and root elongation were prevented in a dose- and time-dependent manner by CdCl₂ treatment. Fluorescence labelling and non-invasive detection showed that CdCl₂ inhibited extracellular Ca²⁺ influx, promoted intracellular Ca²⁺ efflux, and disturbed the cytoplasmic tip-focused Ca²⁺ gradient. In vivo labelling revealed that CdCl₂ modified actin organization, which subsequently contributed to vesicle trafficking. Transmission electron microscopy revealed that CdCl₂ induced cytoplasmic vacuolization and was detrimental to organelles such as mitochondria and endoplasmic reticulum (ER). Finally, immunofluorescent labelling and Fourier transform infrared (FTIR) analysis indicated that configuration/distribution of cell wall components such as pectins and cellulose was significantly altered in response to CdCl₂. Our results indicate that CdCl₂ induces disruption of Ca²⁺ gradient and AFs affects the distribution of cell wall components in root hairs by disturbing vesicular trafficking in A. thaliana.

摘要

镉(Cd)是毒性最大的重金属之一,它能抑制植物中的许多细胞和生理过程。在这里,研究了 CdCl₂处理对拟南芥根(毛)发育过程中液泡运输、细胞壁沉积和尖端生长的细胞质 Ca²⁺梯度和肌动蛋白丝(AFs)的影响。CdCl₂处理以剂量和时间依赖的方式阻止种子萌发和根伸长。荧光标记和非侵入性检测表明,CdCl₂抑制细胞外 Ca²⁺内流,促进细胞内 Ca²⁺外流,并扰乱细胞质尖端聚焦的 Ca²⁺梯度。体内标记显示,CdCl₂改变了肌动蛋白的组织,这随后导致了囊泡运输的改变。透射电子显微镜显示,CdCl₂诱导细胞质空泡化,并对线粒体和内质网(ER)等细胞器造成损害。最后,免疫荧光标记和傅里叶变换红外(FTIR)分析表明,细胞壁成分(如果胶和纤维素)的构象/分布在响应 CdCl₂时发生了显著改变。我们的结果表明,CdCl₂通过干扰拟南芥中的液泡运输,导致 Ca²⁺梯度的破坏和 AFs 的破坏,从而影响根毛中细胞壁成分的分布。

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