An endoplasmic reticulum response pathway mediates programmed cell death of root tip induced by water stress in Arabidopsis
An endoplasmic reticulum response pathway mediates programmed cell death of root tip induced by water stress in Arabidopsis
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DOI：
10.1111/j.1469-8137.2010.03207.x
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发表时间：
2010-01-01
期刊：
影响因子：
9.4
通讯作者：
Li, Xia
中科院分区：
文献类型：
--
作者：
Duan, Yunfeng;Zhang, Wensheng;Li, Xia
P>；干旱诱导植物根死亡，但对根细胞死亡的性质和特征及其潜在的机制还知之甚少。在这里，我们系统地分析了水分胁迫下拟南芥初级根尖的细胞死亡。当达到高水分胁迫时，根尖细胞死亡。死亡细胞首先出现在初生根的顶端分生组织中，并经历了主动的程序性细胞死亡(PCD)。透射电子显微镜分析表明，诱导死亡的细胞具有明显的自噬细胞死亡的形态特征，包括空泡增大，细胞器退化，液泡膜和质膜塌陷。结果表明，自噬PCD的发生是对严重缺水的一种响应，在胁迫的根尖检测到明显的ROS积累。Bax抑制因子-1(AtBI1)在水分胁迫下表达增加，细胞死亡加速，表明AtBI1和内质网(ER)胁迫反应通路共同调控水分胁迫诱导的PCD。这些结果为进一步研究PCD的机制及其在根系构型发育可塑性和随后对水分胁迫的适应中的作用奠定了基础。
P>Drought induces root death in plants; however, the nature and characteristics of root cell death and its underlying mechanisms are poorly understood. Here, we provide a systematic analysis of cell death in the primary root tips in Arabidopsis during water stress.Root tip cell death occurs when high water deficit is reached. The dying cells were first detected in the apical meristem of the primary roots and underwent active programmed cell death (PCD). Transmission electron microscopic analysis shows that the cells undergoing induced death had unambiguous morphological features of autophagic cell death, including an increase in vacuole size, degradation of organelles, and collapse of the tonoplast and the plasma membrane. The results suggest that autophagic PCD occurs as a response to severe water deficit.Significant accumulation of reactive oxygen species (ROS) was detected in the stressed root tips. Expression of BAX inhibitor-1 (AtBI1) was increased in response to water stress, and atbi1-1 displayed accelerated cell death, indicating that AtBI1 and the endoplasmic reticulum (ER) stress response pathway both modulate water stress-induced PCD.These findings form the basis for further investigations into the mechanisms underlying the PCD and its role in developmental plasticity of root system architecture and subsequent adaptation to water stress.