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本文引用的文献

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Fungal attacks on mammalian hosts: pathogen elimination requires sensing and tasting.真菌对哺乳动物宿主的攻击:病原体的消除需要感知和品尝。
Curr Opin Microbiol. 2010 Aug;13(4):401-8. doi: 10.1016/j.mib.2010.05.004. Epub 2010 Jun 9.
2
The Set3/Hos2 histone deacetylase complex attenuates cAMP/PKA signaling to regulate morphogenesis and virulence of Candida albicans.Set3/Hos2 组蛋白去乙酰化酶复合物减弱 cAMP/PKA 信号转导,从而调节白念珠菌的形态发生和毒力。
PLoS Pathog. 2010 May 13;6(5):e1000889. doi: 10.1371/journal.ppat.1000889.
3
Candida albicans hyphal formation and virulence assessed using a Caenorhabditis elegans infection model.使用秀丽隐杆线虫感染模型评估白色念珠菌的菌丝形成和毒力。
Eukaryot Cell. 2009 Nov;8(11):1750-8. doi: 10.1128/EC.00163-09. Epub 2009 Aug 7.
4
Reciprocal regulation of IL-23 and IL-12 following co-activation of Dectin-1 and TLR signaling pathways.在Dectin-1和TLR信号通路共同激活后IL-23和IL-12的相互调节
Eur J Immunol. 2009 May;39(5):1379-86. doi: 10.1002/eji.200838543.
5
Candida albicans cell surface superoxide dismutases degrade host-derived reactive oxygen species to escape innate immune surveillance.白色念珠菌细胞表面超氧化物歧化酶可降解宿主来源的活性氧以逃避天然免疫监视。
Mol Microbiol. 2009 Jan;71(1):240-52. doi: 10.1111/j.1365-2958.2008.06528.x. Epub 2008 Nov 4.
6
Functional mapping of the Candida albicans Efg1 regulator.白色念珠菌Efg1调节因子的功能图谱
Eukaryot Cell. 2008 May;7(5):881-93. doi: 10.1128/EC.00033-08. Epub 2008 Mar 28.
7
Phagocytosis by human neutrophils is stimulated by a unique fungal cell wall component.人类中性粒细胞的吞噬作用受到一种独特的真菌细胞壁成分的刺激。
Cell Host Microbe. 2007 Jul 12;2(1):55-67. doi: 10.1016/j.chom.2007.06.002.
8
Candida albicans Sun41p, a putative glycosidase, is involved in morphogenesis, cell wall biogenesis, and biofilm formation.白色念珠菌Sun41p是一种假定的糖苷酶,参与形态发生、细胞壁生物合成和生物膜形成。
Eukaryot Cell. 2007 Nov;6(11):2056-65. doi: 10.1128/EC.00285-07. Epub 2007 Sep 28.
9
The role of secreted aspartyl proteinases in Candida albicans keratitis.分泌型天冬氨酸蛋白酶在白色念珠菌角膜炎中的作用
Invest Ophthalmol Vis Sci. 2007 Aug;48(8):3559-65. doi: 10.1167/iovs.07-0114.
10
Environmental sensing and signal transduction pathways regulating morphopathogenic determinants of Candida albicans.调节白色念珠菌形态致病决定因素的环境感知与信号转导途径。
Microbiol Mol Biol Rev. 2007 Jun;71(2):348-76. doi: 10.1128/MMBR.00009-06.

转录因子Efg1在调节白色念珠菌的细胞壁结构和免疫原性方面表现出单倍剂量不足表型。

Transcription factor Efg1 shows a haploinsufficiency phenotype in modulating the cell wall architecture and immunogenicity of Candida albicans.

作者信息

Zavrel Martin, Majer Olivia, Kuchler Karl, Rupp Steffen

机构信息

Fraunhofer Institute for Interfacial Engineering and Biotechnology, Stuttgart, Germany.

出版信息

Eukaryot Cell. 2012 Feb;11(2):129-40. doi: 10.1128/EC.05206-11. Epub 2011 Dec 2.

DOI:10.1128/EC.05206-11
PMID:22140230
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3272906/
Abstract

The Candida albicans transcription factor Efg1 is known to be involved in many different cellular processes, including morphogenesis, general metabolism, and virulence. Here we show that besides its manifold roles, Efg1 also has a prominent effect on cell wall structure and composition, strongly affecting the structural glucan part. Deletion of only one allele of EFG1 already results in severe phenotypes for cell wall biogenesis, comparable to those with deletion of both alleles, indicative of a severe haploinsufficiency for EFG1. The observed defects in structural setup of the cell wall, together with previously reported alterations in expression of cell surface proteins, result in altered immunogenic properties of strains with compromised Efg1 function. This is shown by interaction studies with macrophages and primary dendritic cells. The structural changes in the cell wall carbohydrate meshwork presented here, together with the manifold changes in cell wall protein composition and metabolism reported in other studies, contribute to the altered immune response mounted by innate immune cells and to the altered virulence phenotypes observed for strains lacking EFG1.

摘要

已知白色念珠菌转录因子Efg1参与许多不同的细胞过程,包括形态发生、一般代谢和毒力。在此我们表明,除了其多种作用外,Efg1对细胞壁结构和组成也有显著影响,强烈影响结构葡聚糖部分。仅缺失EFG1的一个等位基因就已导致细胞壁生物合成出现严重表型,与缺失两个等位基因的情况相当,表明EFG1存在严重的单倍体不足。观察到的细胞壁结构设置缺陷,连同先前报道的细胞表面蛋白表达改变,导致Efg1功能受损菌株的免疫原性特性发生改变。与巨噬细胞和原代树突状细胞的相互作用研究表明了这一点。此处呈现的细胞壁碳水化合物网络结构变化,连同其他研究报道的细胞壁蛋白质组成和代谢的多种变化,导致先天免疫细胞引发的免疫反应改变,以及缺乏EFG1的菌株所观察到的毒力表型改变。