Endoplasmic reticulum stress and fungal pathogenesis

被引:37
作者
Krishnan, Karthik [1 ]
Askew, David S. [1 ]
机构
[1] Univ Cincinnati, Dept Pathol & Lab Med, Cincinnati, OH 45267 USA
基金
美国国家卫生研究院;
关键词
ER stress; Fungal pathogenesis; Fungal virulence; Hac1; HacA; Ire1; IreA; Unfolded protein response; UPR; UNFOLDED-PROTEIN RESPONSE; ER-ASSOCIATED DEGRADATION; ASPERGILLUS-FUMIGATUS; CRYPTOCOCCUS-NEOFORMANS; CANDIDA-ALBICANS; SACCHAROMYCES-CEREVISIAE; MAGNAPORTHE-ORYZAE; FILAMENTOUS FUNGI; HOST TEMPERATURE; SECRETION STRESS;
D O I
10.1016/j.fbr.2014.07.001
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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. (C) 2014 The British Mycological Society. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:29 / 35
页数:7
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