Genetic interactions between KAR2 and SEC63, encoding eukaryotic homologues of DnaK and DnaJ in the endoplasmic reticulum.
Genetic interactions between KAR2 and SEC63, encoding eukaryotic homologues of DnaK and DnaJ in the endoplasmic reticulum.
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DOI：
10.1091/mbc.4.11.1145
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发表时间：
1993-11
影响因子：
3.3
通讯作者：
M. Scidmore;Heid H. Okamura;M. Rose
中科院分区：
文献类型：
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作者：
M. Scidmore;Heid H. Okamura;M. Rose
KAR 2编码哺乳动物BiP的酵母同源物，BiP是HSP 70家族的内质网（ER）驻留成员。Kar 2 p已被证明是蛋白质跨ER膜转运以及核融合所必需的。Sec 63是一种与大肠杆菌DnaJ蛋白同源的ER整合膜蛋白，也是易位所需的。在本文中，我们描述了这两个蛋白质，Kar 2 p和Sec 63 p之间的几个特定的遗传相互作用。首先，KAR 2和SEC 63中的温度敏感突变形成合成的致命组合。其次，KAR 2的显性突变是sec 63 -1的温度敏感性生长和易位缺陷的等位基因特异性抑制因子。第三，sec 63 -1与其他易位缺陷突变不同，导致KAR 2 mRNA水平的诱导。综上所述，这些遗传相互作用表明Kar 2 p和Sec 63 p在体内以类似于E. coli HSP 70、DnaK和DnaJ。我们建议，这两种蛋白质之间的相互作用是至关重要的，它们的功能在蛋白质易位。
KAR2 encodes the yeast homologue of mammalian BiP, the endoplasmic reticulum (ER) resident member of the HSP70 family. Kar2p has been shown to be required for the translocation of proteins across the ER membrane as well as nuclear fusion. Sec63, an ER integral membrane protein that shares homology with the Escherichia coli DnaJ protein, is also required for translocation. In this paper we describe several specific genetic interactions between these two proteins, Kar2p and Sec63p. First, temperature-sensitive mutations in KAR2 and SEC63 form synthetic lethal combinations. Second, dominant mutations in KAR2 are allele-specific suppressors for the temperature-sensitive growth and translocation defect of sec63-1. Third, the sec63-1, unlike other translocation defective mutations, results in the induction of KAR2 mRNA levels. Taken together, these genetic interactions suggest that Kar2p and Sec63p interact in vivo in a manner similar to that of the E. coli HSP70, DnaK, and DnaJ. We propose that the interaction between these two proteins is critical to their function in protein translocation.