Endoplasmic reticulum stress and fungal pathogenesis.
Endoplasmic reticulum stress and fungal pathogenesis.
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DOI：
10.1016/j.fbr.2014.07.001
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发表时间：
2014-10-01
影响因子：
6
通讯作者：
Askew, David S.
中科院分区：
文献类型：
--
作者：
Krishnan, Karthik;Askew, David S.
通往分泌途径的门户是内质网（ER），内质网是负责多达三分之一的细胞蛋白质组的准确折叠、翻译后修饰和最终组装的细胞器。当分泌水平高时，蛋白质生物合成中的错误可导致异常折叠蛋白质的积累，这威胁到ER稳态。未折叠蛋白反应（UPR）是一种适应性信号通路，通过增加支持ER蛋白折叠能力的基因表达来对抗错误折叠和未折叠蛋白的积累。真菌，像其他真核细胞，是专门为分泌，依赖于UPR缓冲ER压力所造成的波动分泌的需求。然而，新出现的证据也暗示UPR作为真菌发病机制的中央调节器。在这篇综述中，我们讨论了不同的真菌病原体如何适应ER应激反应途径，以支持在宿主环境中所必需的毒力相关性状的表达。
The gateway to the secretory pathway is the endoplasmic reticulum (ER), an organelle that is responsible for the accurate folding, post-translational modification and final assembly of up to a third of the cellular proteome. When secretion levels are high, errors in protein biogenesis can lead to the accumulation of abnormally folded proteins, which threaten ER homeostasis. The unfolded protein response (UPR) is an adaptive signaling pathway that counters a buildup in misfolded and unfolded proteins by increasing the expression of genes that support ER protein folding capacity. Fungi, like other eukaryotic cells that are specialized for secretion, rely upon the UPR to buffer ER stress caused by fluctuations in secretory demand. However, emerging evidence is also implicating the UPR as a central regulator of fungal pathogenesis. In this review, we discuss how diverse fungal pathogens have adapted ER stress response pathways to support the expression of virulence-related traits that are necessary in the host environment.
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