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
Institute of Molecular Cell Biology, BioCentrum Amsterdam, University of Amsterdam, The Netherlands.
J Bacteriol. 1998 Mar;180(6):1418-24. doi: 10.1128/JB.180.6.1418-1424.1998.
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.
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。