Berrier C, Garrigues A, Richarme G, Ghazi A
Laboratoire des Biomembranes, UMR CNRS 8619, Université Paris-Sud, 91405 Orsay Cedex, France.
J Bacteriol. 2000 Jan;182(1):248-51. doi: 10.1128/JB.182.1.248-251.2000.
Upon osmotic downshock, a few cytoplasmic proteins, including thioredoxin, elongation factor Tu (EF-Tu), and DnaK, are released from Tris-EDTA-treated Escherichia coli cells by an unknown mechanism. We have shown previously that deletion of mscL, the gene coding for the mechanosensitive channel of the plasma membrane with the highest conductance, prevents the release of thioredoxin. We confirm and extend the implication of MscL in this process by showing that the release of EF-Tu and DnaK is severely impaired in MscL-deficient strains. Release of these proteins is not observed in the absence of a Tris-EDTA treatment which disrupts the outer membrane, indicating that, in intact cells, they are transferred to the periplasm upon shock, presumably through the MscL channel.
在渗透减压冲击下,包括硫氧还蛋白、延伸因子Tu(EF-Tu)和DnaK在内的一些细胞质蛋白会通过一种未知机制从经Tris-EDTA处理的大肠杆菌细胞中释放出来。我们之前已经表明,编码质膜中电导最高的机械敏感通道的基因mscL缺失,会阻止硫氧还蛋白的释放。我们通过证明在缺乏MscL的菌株中EF-Tu和DnaK的释放严重受损,证实并扩展了MscL在此过程中的作用。在没有破坏外膜的Tris-EDTA处理的情况下,未观察到这些蛋白质的释放,这表明在完整细胞中,它们在冲击时会转移到周质中,大概是通过MscL通道。