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本文引用的文献

1
Altered extent of cross-linking of beta1,6-glucosylated mannoproteins to chitin in Saccharomyces cerevisiae mutants with reduced cell wall beta1,3-glucan content.在细胞壁β1,3-葡聚糖含量降低的酿酒酵母突变体中,β1,6-葡萄糖基化甘露糖蛋白与几丁质交联程度的改变。
J Bacteriol. 1997 Oct;179(20):6279-84. doi: 10.1128/jb.179.20.6279-6284.1997.
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Architecture of the yeast cell wall. Beta(1-->6)-glucan interconnects mannoprotein, beta(1-->)3-glucan, and chitin.酵母细胞壁的结构。β(1→6)-葡聚糖连接甘露糖蛋白、β(1→3)-葡聚糖和几丁质。
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Increase in chitin as an essential response to defects in assembly of cell wall polymers in the ggp1delta mutant of Saccharomyces cerevisiae.在酿酒酵母ggp1delta突变体中,几丁质增加是对细胞壁聚合物组装缺陷的一种重要反应。
J Bacteriol. 1997 Jan;179(2):463-9. doi: 10.1128/jb.179.2.463-469.1997.
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The PMT gene family: protein O-glycosylation in Saccharomyces cerevisiae is vital.PMT基因家族:酿酒酵母中的蛋白质O-糖基化至关重要。
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Measurement of beta(1-->3)-glucans in occupational and home environments with an inhibition enzyme immunoassay.采用抑制酶免疫分析法测定职业环境和家庭环境中的β(1→3)-葡聚糖。
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Retention of Saccharomyces cerevisiae cell wall proteins through a phosphodiester-linked beta-1,3-/beta-1,6-glucan heteropolymer.通过磷酸二酯连接的β-1,3-/β-1,6-葡聚糖杂聚物保留酿酒酵母细胞壁蛋白。
Glycobiology. 1996 Apr;6(3):337-45. doi: 10.1093/glycob/6.3.337.
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In vitro activity of 1,3-beta-D-glucan synthase requires the GTP-binding protein Rho1.1,3-β-D-葡聚糖合酶的体外活性需要GTP结合蛋白Rho1。
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Activation of yeast protein kinase C by Rho1 GTPase.Rho1 GTP酶对酵母蛋白激酶C的激活作用。
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Identification of yeast Rho1p GTPase as a regulatory subunit of 1,3-beta-glucan synthase.鉴定酵母Rho1p GTP酶为1,3-β-葡聚糖合酶的调节亚基。
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Rho1p, a yeast protein at the interface between cell polarization and morphogenesis.Rho1p,一种处于细胞极化与形态发生界面的酵母蛋白。
Science. 1996 Apr 12;272(5259):277-9. doi: 10.1126/science.272.5259.277.

酿酒酵母中质膜结合蛋白Gas1p的缺失会导致β-1,3-葡聚糖释放到培养基中,并诱导一种补偿机制以确保细胞壁的完整性。

Loss of the plasma membrane-bound protein Gas1p in Saccharomyces cerevisiae results in the release of beta1,3-glucan into the medium and induces a compensation mechanism to ensure cell wall integrity.

作者信息

Ram A F, Kapteyn J C, Montijn R C, Caro L H, Douwes J E, Baginsky W, Mazur P, van den Ende H, Klis F M

机构信息

Institute of Molecular Cell Biology, BioCentrum Amsterdam, University of Amsterdam, The Netherlands.

出版信息

J Bacteriol. 1998 Mar;180(6):1418-24. doi: 10.1128/JB.180.6.1418-1424.1998.

DOI:10.1128/JB.180.6.1418-1424.1998
PMID:9515908
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC107039/
Abstract

Deletion of GAS1/GGP1/CWH52 results in a lower beta-glucan content of the cell wall and swollen, more spherical cells (L. Popolo, M. Vai, E. Gatti, S. Porello, P. Bonfante, R. Balestrini, and L. Alberghina, J. Bacteriol. 175:1879-1885, 1993; A. F. J. Ram, S. S. C. Brekelmans, L. J. W. M. Oehlen, and F. M. Klis, FEBS Lett. 358:165-170, 1995). We show here that gas1delta cells release beta1,3-glucan into the medium. Western analysis of the medium proteins with beta1,3-glucan- and beta1,6-glucan-specific antibodies showed further that at least some of the released beta1,3-glucan was linked to protein as part of a beta1,3-glucan-beta1,6-glucan-protein complex. These data indicate that Gas1p might play a role in the retention of beta1,3-glucan and/or beta-glucosylated proteins. Interestingly, the defective incorporation of beta1,3-glucan in the cell wall was accompanied by an increase in chitin and mannan content in the cell wall, an enhanced expression of cell wall protein 1 (Cwp1p), and an increase in beta1,3-glucan synthase activity, probably caused by the induced expression of Fks2p. It is proposed that the cell wall weakening caused by the loss of Gas1p induces a set of compensatory reactions to ensure cell integrity.

摘要

GAS1/GGP1/CWH52基因的缺失会导致细胞壁中β-葡聚糖含量降低,细胞肿胀且更接近球形(L. 波波洛、M. 瓦伊、E. 加蒂、S. 波雷洛、P. 邦方特、R. 巴莱斯特里尼和L. 阿尔贝吉纳,《细菌学杂志》175:1879 - 1885,1993;A. F. J. 拉姆、S. S. C. 布雷克曼斯、L. J. W. M. 奥伦和F. M. 克利斯,《欧洲生物化学学会联合会快报》358:165 - 170,1995)。我们在此表明,gas1delta细胞会将β1,3 - 葡聚糖释放到培养基中。用β1,3 - 葡聚糖和β1,6 - 葡聚糖特异性抗体对培养基蛋白进行的蛋白质免疫印迹分析进一步表明,至少一些释放的β1,3 - 葡聚糖与蛋白质相连,作为β1,3 - 葡聚糖 - β1,6 - 葡聚糖 - 蛋白质复合物的一部分。这些数据表明Gas1p可能在β1,3 - 葡聚糖和/或β - 葡糖基化蛋白的保留中发挥作用。有趣的是,细胞壁中β1,3 - 葡聚糖掺入缺陷伴随着细胞壁中几丁质和甘露聚糖含量的增加、细胞壁蛋白1(Cwp1p)表达的增强以及β1,3 - 葡聚糖合酶活性的增加,这可能是由Fks2p的诱导表达引起的。有人提出,Gas1p缺失导致的细胞壁弱化会引发一系列补偿反应以确保细胞完整性。