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编码具有预测转糖苷酶结构域的细胞壁糖基磷脂酰肌醇蛋白的CRH家族影响白色念珠菌的细胞壁组织和毒力。

The CRH family coding for cell wall glycosylphosphatidylinositol proteins with a predicted transglycosidase domain affects cell wall organization and virulence of Candida albicans.

作者信息

Pardini Giacomo, De Groot Piet W J, Coste Alix T, Karababa Mahir, Klis Frans M, de Koster Chris G, Sanglard Dominique

机构信息

Institute of Microbiology, University Hospital Lausanne, CH-1011 Lausanne, Switzerland.

出版信息

J Biol Chem. 2006 Dec 29;281(52):40399-411. doi: 10.1074/jbc.M606361200. Epub 2006 Oct 30.

Abstract

In Candida albicans UTR2 (CSF4), CRH11, and CRH12 are members of a gene family (the CRH family) that encode glycosylphosphatidylinositol-dependent cell wall proteins with putative transglycosidase activity. Deletion of genes of this family resulted in additive sensitivity to compounds interfering with normal cell wall formation (Congo red, calcofluor white, SDS, and high Ca(2+) concentrations), suggesting that these genes contribute to cell wall organization. A triple mutant lacking UTR2, CRH11, and CRH12 produced a defective cell wall, as inferred from increased sensitivity to cell wall-degrading enzymes, decreased ability of protoplasts to regenerate a new wall, constitutive activation of Mkc1p, the mitogen-activated protein kinase of the cell wall integrity pathway, and an increased chitin content of the cell wall. Importantly, this was accompanied by a decrease in alkali-insoluble 1,3-beta-glucan but not total glucan content, suggesting that formation of the linkage between 1,3-beta-glucan and chitin might be affected. In support of this idea, localization of a Utr2p-GFP fusion protein largely coincided with areas of chitin incorporation in C. albicans. As UTR2 and CRH11 expression is regulated by calcineurin, a serine/threonine protein phosphatase involved in tolerance to antifungal drugs, cell wall morphogenesis, and virulence, this points to a possible relationship between calcineurin and the CRH family. Deletion of UTR2, CRH11, and CRH12 resulted in only a partial overlap with calcineurin-dependent phenotypes, suggesting that calcineurin has additional targets. Interestingly, cells deleted for UTR2, CRH11, and CRH12 were, like a calcineurin mutant, avirulent in a mouse model of systemic infection but retained the capacity to colonize target organs (kidneys) as the wild type. In conclusion, this work establishes the role of UTR2, CRH11, and CRH12 in cell wall organization and integrity.

摘要

在白色念珠菌中,UTR2(CSF4)、CRH11和CRH12是一个基因家族(CRH家族)的成员,该家族编码具有假定转糖基酶活性的糖基磷脂酰肌醇依赖性细胞壁蛋白。该家族基因的缺失导致对干扰正常细胞壁形成的化合物(刚果红、荧光增白剂、十二烷基硫酸钠和高钙浓度)的累加敏感性,表明这些基因有助于细胞壁的组织。缺乏UTR2、CRH11和CRH12的三重突变体产生了有缺陷的细胞壁,这可从对细胞壁降解酶的敏感性增加、原生质体再生新壁的能力降低、细胞壁完整性途径的丝裂原活化蛋白激酶Mkc1p的组成型激活以及细胞壁几丁质含量增加推断出来。重要的是,这伴随着碱不溶性1,3-β-葡聚糖的减少,但总葡聚糖含量未减少,表明1,3-β-葡聚糖和几丁质之间的连接形成可能受到影响。支持这一观点的是,Utr2p-GFP融合蛋白的定位在很大程度上与白色念珠菌中几丁质掺入的区域一致。由于UTR2和CRH11的表达受钙调神经磷酸酶调节,钙调神经磷酸酶是一种参与抗真菌药物耐受性、细胞壁形态发生和毒力的丝氨酸/苏氨酸蛋白磷酸酶,这表明钙调神经磷酸酶与CRH家族之间可能存在关系。UTR2、CRH11和CRH12的缺失仅导致与钙调神经磷酸酶依赖性表型的部分重叠,表明钙调神经磷酸酶还有其他靶点。有趣的是,缺失UTR2、CRH11和CRH12的细胞与钙调神经磷酸酶突变体一样,在系统性感染的小鼠模型中无毒力,但保留了像野生型一样定殖于靶器官(肾脏)的能力。总之,这项工作确定了UTR2、CRH11和CRH12在细胞壁组织和完整性中的作用。

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