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自我与非我:木霉中真菌细胞壁的降解。

Self versus non-self: fungal cell wall degradation in Trichoderma.

机构信息

Research Area Gene Technology and Applied Biochemistry, Institute of Chemical Engineering, Vienna University of Technology, Gumpendorfer Strasse 1a, 1060 Vienna, Austria.

出版信息

Microbiology (Reading). 2012 Jan;158(Pt 1):26-34. doi: 10.1099/mic.0.052613-0. Epub 2011 Aug 26.

DOI:10.1099/mic.0.052613-0
PMID:21873410
Abstract

Lysis of the prey's cell wall is one of the key steps during mycoparasitism. Genome analysis of two mycoparasitic Trichoderma species, T. atroviride and T. virens, revealed an expanded arsenal of genes encoding enzymes potentially involved in cell wall hydrolysis. Glycoside hydrolase family 18, which contains all fungal chitinases, is the largest family of carbohydrate-active enzymes in mycoparasitic Trichoderma species. However, in addition to their aggressive functions during mycoparasitism, the roles of chitinases and other cell wall degrading enzymes also include remodelling and recycling of the fungus's own cell wall. In this review we discuss current knowledge about fungal cell wall degrading enzymes in Trichoderma and how the fungus distinguishes between self- and non-self fungal cell wall degradation. In the past few years, the chitinolytic enzyme machinery of Trichoderma has been used as a model system to address this question. Gene expression profiles of most investigated chitinases indicate an overlap of functions of the respective enzymes and an involvement in both self- and non-self fungal cell wall degradation. Similar sets of enzymes appear to be involved in mycoparasitism, exogenous chitin decomposition and recycling of the fungus's own cell wall. Thus, we hypothesize that the regulation of self and non-self fungal cell wall degradation is not due to a speciation of individual chitinases. Rather, we hypothesize that it is regulated by substrate accessibility due to cell wall protection in healthy hyphae vs deprotection during mycoparasitic attack, hyphal ageing and autolysis.

摘要

猎物细胞壁的溶解是菌寄生作用的关键步骤之一。对两种菌寄生性木霉(T. atroviride 和 T. virens)的基因组分析揭示了一个扩展的基因武器库,这些基因编码潜在参与细胞壁水解的酶。糖苷水解酶家族 18 包含所有真菌几丁质酶,是菌寄生性木霉中最大的碳水化合物活性酶家族。然而,除了在菌寄生作用中具有攻击性的功能外,几丁质酶和其他细胞壁降解酶的作用还包括真菌自身细胞壁的重塑和再循环。在这篇综述中,我们讨论了真菌细胞壁降解酶在木霉中的最新知识,以及真菌如何区分自身和非自身真菌细胞壁的降解。在过去的几年中,木霉的几丁质酶酶解机制已被用作模型系统来解决这个问题。大多数研究的几丁质酶的基因表达谱表明,各自酶的功能重叠,并参与自身和非自身真菌细胞壁的降解。类似的酶似乎参与菌寄生作用、外源几丁质分解和真菌自身细胞壁的再循环。因此,我们假设自身和非自身真菌细胞壁降解的调节不是由于单个几丁质酶的特化。相反,我们假设它是由细胞壁保护下的底物可及性调节的,在健康菌丝中存在细胞壁保护,而在菌寄生攻击、菌丝老化和自溶期间则不存在细胞壁保护。

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