Fang H, Green N
Department of Microbiology and Immunology, School of Medicine, Vanderbilt University, Nashville, Tennessee 37232-2363.
Mol Biol Cell. 1994 Sep;5(9):933-42. doi: 10.1091/mbc.5.9.933.
The sec71-1 and sec72-1 mutations were identified by a genetic assay that monitored membrane protein integration into the endoplasmic reticulum (ER) membrane of the yeast Saccharomyces cerevisiae. The mutations inhibited integration of various chimeric membrane proteins and translocation of a subset of water soluble proteins. In this paper we show that SEC71 encodes the 31.5-kDa transmembrane glycoprotein (p31.5) and SEC72 encodes the 23-kDa protein (p23) of the Sec63p-BiP complex. SEC71 is therefore identical to SEC66 (HSS1), which was previously shown to encode p31.5. DNA sequence analyses reveal that sec71-1 cells contain a nonsense mutation that removes approximately two-thirds of the cytoplasmic C-terminal domain of p31.5. The sec72-1 mutation shifts the reading frame of the gene encoding p23. Unexpectedly, the sec71-1 mutant lacks p31.5 and p23. Neither mutation is lethal, although sec71-1 cells exhibit a growth defect at 37 degrees C. These results show that p31.5 and p23 are important for the trafficking of a subset of proteins to the ER membrane.
sec71-1和sec72-1突变是通过一种遗传检测方法鉴定出来的，该方法监测膜蛋白整合到酿酒酵母内质网（ER）膜中的情况。这些突变抑制了各种嵌合膜蛋白的整合以及一部分水溶性蛋白的转运。在本文中，我们表明SEC71编码Sec63p-BiP复合体的31.5 kDa跨膜糖蛋白（p31.5），SEC72编码23 kDa蛋白（p23）。因此，SEC71与先前显示编码p31.5的SEC66（HSS1）相同。DNA序列分析表明，sec71-1细胞含有一个无义突变，该突变去除了p31.5约三分之二的胞质C末端结构域。sec72-1突变改变了编码p23的基因的阅读框。出乎意料的是，sec71-1突变体缺乏p31.5和p23。尽管sec71-1细胞在37℃时表现出生长缺陷，但这两种突变都不是致死性的。这些结果表明，p31.5和p23对于一部分蛋白转运到ER膜是重要的。
