Kontinen V P, Tokuda H
Institute of Molecular and Cellular Biosciences, University of Tokyo, Japan.
FEBS Lett. 1995 May 8;364(2):157-60. doi: 10.1016/0014-5793(95)00378-m.
The E. coli secG deletion mutant is unable to grow and is defective in protein translocation at low temperature. A gene of Bacillus subtilis, which is able to restore the growth of the deletion mutant at low temperature, was found as a multi-copy suppressor. Sequencing of this gene revealed significant homology to E. coli pgsA, which encodes phosphatidylglycerophosphate synthase, an enzyme involved in acidic phospholipid synthesis. A plasmid carrying E. coli pgsA also restored the growth of the deletion mutant. Furthermore, protein translocation in the deletion mutant was stimulated when it harbored a plasmid carrying pgsA. A possible mechanism underlying the pgsA-dependent suppression of the secG deletion mutation is discussed.
大肠杆菌secG缺失突变体无法生长，且在低温下蛋白质转运存在缺陷。发现枯草芽孢杆菌的一个基因作为多拷贝抑制子，能够恢复该缺失突变体在低温下的生长。对该基因进行测序后发现，它与大肠杆菌pgsA具有显著同源性，pgsA编码磷脂酰甘油磷酸合酶，这是一种参与酸性磷脂合成的酶。携带大肠杆菌pgsA的质粒也能恢复缺失突变体的生长。此外，当缺失突变体携带携带pgsA的质粒时，其蛋白质转运受到刺激。本文讨论了pgsA依赖型抑制secG缺失突变的可能机制。
