When supply does not meet demand-ER stress and plant programmed cell death.
When supply does not meet demand-ER stress and plant programmed cell death.
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DOI：
10.3389/fpls.2014.00211
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发表时间：
2014
影响因子：
5.6
通讯作者：
Dickman MB
中科院分区：
文献类型：
--
作者：
Williams B;Verchot J;Dickman MB
内质网是真核细胞分泌途径的中心细胞器。ER在蛋白质合成和成熟中起作用，并且对于适当维持细胞稳态和适应不利环境至关重要。作为细胞的哨兵，ER对变化的环境非常敏感，主要是通过ER质量控制机制。当受到干扰时，ER应激会触发一个被称为未折叠蛋白反应（UPR）的严格调节和高度保守的信号转导途径，该途径可防止未折叠/错误折叠蛋白的危险积累。在过量的UPR活性超过阈值水平的情况下，细胞恶化并最终触发程序性细胞死亡（PCD），作为生物体科普功能失调或毒性信号的一种方式。在哺乳动物系统中，由于过度的ER应激而导致的程序性细胞死亡有助于几种重要的疾病，包括缺氧、神经变性和糖尿病。重要的是，在哺乳动物中与ER应激相关的细胞死亡的标志性特征和标记物也在植物中发现。特别是，有一个共同的，保守的一组分子伴侣，调节ER细胞死亡信号。在这里，我们回顾了植物细胞死亡响应ER压力的元素，并注意到越来越多的植物-病原体相互作用正在确定其中宿主ER是植物病原体的目标，以建立兼容性。
The endoplasmic reticulum (ER) is the central organelle in the eukaryotic secretory pathway. The ER functions in protein synthesis and maturation and is crucial for proper maintenance of cellular homeostasis and adaptation to adverse environments. Acting as a cellular sentinel, the ER is exquisitely sensitive to changing environments principally via the ER quality control machinery. When perturbed, ER-stress triggers a tightly regulated and highly conserved, signal transduction pathway known as the unfolded protein response (UPR) that prevents the dangerous accumulation of unfolded/misfolded proteins. In situations where excessive UPR activity surpasses threshold levels, cells deteriorate and eventually trigger programmed cell death (PCD) as a way for the organism to cope with dysfunctional or toxic signals. The programmed cell death that results from excessive ER stress in mammalian systems contributes to several important diseases including hypoxia, neurodegeneration, and diabetes. Importantly, hallmark features and markers of cell death that are associated with ER stress in mammals are also found in plants. In particular, there is a common, conserved set of chaperones that modulate ER cell death signaling. Here we review the elements of plant cell death responses to ER stress and note that an increasing number of plant-pathogen interactions are being identified in which the host ER is targeted by plant pathogens to establish compatibility.
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