Shim J, Newman A P, Ferro-Novick S
Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, Connecticut 06510.
J Cell Biol. 1991 Apr;113(1):55-64. doi: 10.1083/jcb.113.1.55.
We recently described the identification of BOS1 (Newman, A., J. Shim, and S. Ferro-Novick. 1990. Mol. Cell. Biol. 10:3405-3414.). BOS1 is a gene that in multiple copy suppresses the growth and secretion defect of bet1 and sec22, two mutants that disrupt transport from the ER to the Golgi complex in yeast. The ability of BOS1 to specifically suppress mutants blocked at a particular stage of the secretory pathway suggested that this gene encodes a protein that functions in this process. The experiments presented in this study support this hypothesis. Specifically, the BOS1 gene was found to be essential for cellular growth. Furthermore, cells depleted of the Bos1 protein fail to transport pro-alpha-factor and carboxypeptidase Y (CPY) to the Golgi apparatus. This defect in export leads to the accumulation of an extensive network of ER and small vesicles. DNA sequence analysis predicts that Bos1 is a 27-kD protein containing a putative membrane-spanning domain. This prediction is supported by differential centrifugation experiments. Thus, Bos1 appears to be a membrane protein that functions in conjunction with Bet1 and Sec22 to facilitate the transport of proteins at a step subsequent to translocation into the ER but before entry into the Golgi apparatus.
我们最近描述了BOS1的鉴定(纽曼,A.,J. 沈,和S. 费罗-诺维克。1990年。《分子与细胞生物学》10:3405 - 3414)。BOS1是一个基因,其多拷贝形式可抑制bet1和sec22的生长和分泌缺陷,这两个突变体破坏了酵母中从内质网到高尔基体复合体的转运。BOS1特异性抑制在分泌途径特定阶段受阻的突变体的能力表明,该基因编码一种在此过程中发挥作用的蛋白质。本研究中的实验支持了这一假设。具体而言,发现BOS1基因对细胞生长至关重要。此外,缺乏Bos1蛋白的细胞无法将前α因子和羧肽酶Y(CPY)转运到高尔基体。这种输出缺陷导致内质网和小泡的广泛网络积累。DNA序列分析预测Bos1是一种含有推定跨膜结构域的27-kD蛋白。这一预测得到了差速离心实验的支持。因此,Bos1似乎是一种膜蛋白,它与Bet1和Sec22协同作用,在蛋白质转运到内质网之后但进入高尔基体之前的步骤中促进蛋白质的转运。