SUPPRESSION OF A SEC63 MUTATION IDENTIFIES A NOVEL COMPONENT OF THE YEAST ENDOPLASMIC-RETICULUM TRANSLOCATION APPARATUS
SUPPRESSION OF A SEC63 MUTATION IDENTIFIES A NOVEL COMPONENT OF THE YEAST ENDOPLASMIC-RETICULUM TRANSLOCATION APPARATUS
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DOI：
10.1091/mbc.4.9.919
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发表时间：
1993-09-01
影响因子：
3.3
通讯作者：
SILVER, P
中科院分区：
文献类型：
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作者：
KURIHARA, T;SILVER, P
SEC 63基因的突变与蛋白质转运到内质网（ER）中的缺陷以及酿酒酵母中核蛋白定位的缺陷有关。为了鉴定可能与SEC 63 p相互作用和/或起作用的蛋白质，我们克隆了SEC 63 -101突变体的温度敏感致死表型的高拷贝抑制子（HSS 1）。HSS 1是一个等位基因特异性的sec 63抑制基因，编码一个完整的ER膜糖蛋白，其N-末端位于ER腔，C-末端位于细胞质中。HSS 1破坏的单倍体菌株对生长和积累Kar 2 p和转化酶的前体形式是温度敏感的。HSS 1无效等位基因与影响ER易位的突变组合是合成致死的。我们建议，HSS 1 p是重要的ER易位和相互作用与先前确定的组件的酵母易位装置。HSS 1与SEC 66相同，后者编码与SEC 62 p和SEC 63 p复合的糖蛋白。
Mutations in the SEC63 gene are associated with defects in protein translocation into the endoplasmic reticulum (ER) as well as in nuclear protein localization in Saccharomyces cerevisiae. To identify proteins that might interact and/or function with SEC63p, we cloned a high copy suppressor (HSS1) of the temperature-sensitive lethal phenotype of the sec63-101 mutant. HSS1 is an allele-specific sec63 suppressor that encodes an integral ER membrane glycoprotein of 206 amino acids with the N-terminus in the ER lumen and C-terminal region in the cytoplasm. Haploid strains disrupted for HSS1 are temperature-sensitive for growth and accumulate precursor forms of Kar2p and invertase. The HSS1 null allele is synthetically lethal in combination with mutations affecting ER translocation. We propose that HSS1p is important for ER translocation and interacts with previously identified components of the yeast translocation apparatus. HSS1 is identical to SEC66, which encodes a glycoprotein complexed with SEC62p and SEC63p.