ERD1, A YEAST GENE REQUIRED FOR THE RETENTION OF LUMINAL ENDOPLASMIC-RETICULUM PROTEINS, AFFECTS GLYCOPROTEIN PROCESSING IN THE GOLGI-APPARATUS
ERD1, A YEAST GENE REQUIRED FOR THE RETENTION OF LUMINAL ENDOPLASMIC-RETICULUM PROTEINS, AFFECTS GLYCOPROTEIN PROCESSING IN THE GOLGI-APPARATUS
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DOI：
10.1002/j.1460-2075.1990.tb08154.x
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发表时间：
1990-03-01
期刊：
影响因子：
11.4
通讯作者：
PELHAM, HRB
中科院分区：
文献类型：
--
作者：
HARDWICK, KG;LEWIS, MJ;PELHAM, HRB
我们之前已经证明，C 端序列 HDEL 充当酿酒酵母中管腔内质网 (ER) 蛋白的保留信号，并且可以分离出无法保留带有此信号的转化酶融合蛋白的突变体。对许多此类突变体的分析定义了两个基因：ERD1 和 ERD2。缺乏 ERD1 基因的细胞会分泌内源性 ER 蛋白 BiP。在正常生长条件下，分泌速率相当于野生型细胞分泌完全缺乏 HDEL 信号的修饰形式 BiP 的速率。因此，erd1 细胞显示出保留系统的严重破坏。突变细胞的细胞内膜系统没有明显的异常，但糖蛋白的高尔基依赖性修饰存在缺陷。我们认为管腔 ER 蛋白的分类通常发生在高尔基体中，并且 ERD1 的功能是 HDEL 受体与其配体正确相互作用所必需的。 ERD1 的序列预测具有多个跨膜结构域的膜蛋白，这一结论得到了 ERD1-SUC2 融合蛋白分析的支持。
We have previously shown that the C-terminal sequence HDEL acts as a retention signal for luminal endoplasmic reticulum (ER) proteins in Saccharomyces cerevisiae, and that it is possible to isolate mutants that fail to retain an invertase fusion protein bearing this signal. Analysis of many such mutants defines two genes, ERD1 and ERD2. Cells lacking the ERD1 gene secrete the endogenous ER protein, BiP. Under normal growth conditions, the rate of secretion is equivalent to the rate at which wild-type cells secrete a modified form of BiP that lacks the HDEL signal altogether. Thus, erd1 cells show a profound disruption of the retention system. The mutant cells have no gross abnormality of their intracellular membrane system, but show defects in the Golgi-dependent modification of glycoproteins. We suggest that sorting of luminal ER proteins normally occurs in the Golgi, and that the function of ERD1 is required for the correct interaction of an HDEL receptor with its ligands. The sequence of ERD1 predicts a membrane protein with several transmembrane domains, a conclusion supported by analysis of ERD1-SUC2 fusion proteins.