CNRS UPR9073 associated with University Paris VII, Institut de Biologie Physico-chimique, 13 rue Pierre et Marie Curie 75005 Paris, France.
Mol Microbiol. 2011 Jan;79(2):288-91. doi: 10.1111/j.1365-2958.2010.07468.x. Epub 2010 Nov 29.
In this issue of Molecular Microbiology, Schaub and Hayes report that, compared with other enterobacteria, Escherichia coli K12 carries two mutations - one in the prfB gene encoding the release factor RF2, and the other in the rpsG gene encoding r-protein S7 - that together concur in compromising translation termination at the essential rpsG gene. As a consequence, the growth of E. coli K12 is very sensitive to a further mutation (rluD(-) ) that depresses RF2 activity, whereas the growth of its close relative, E. coli B, is not. We tentatively discuss how the K12-specific mutations in RF2 and S7 might have occurred and why inefficient translation termination at rpsG inhibits growth. The work of Schaub and Hayes illustrates the fact that, due probably to its long history in the laboratory, E. coli K12 has accumulated mutations that sometimes limit its value as a model for studying basic steps in prokaryotic gene expression.
在本期《分子微生物学》中，Schaub 和 Hayes 报道称，与其他肠杆菌相比，大肠杆菌 K12 携带两个突变——一个在编码释放因子 RF2 的 prfB 基因中，另一个在编码 r 蛋白 S7 的 rpsG 基因中——这两个突变共同导致必需的 rpsG 基因的翻译终止受到影响。因此，大肠杆菌 K12 的生长对进一步降低 RF2 活性的突变（rluD(-)）非常敏感，而其近亲大肠杆菌 B 的生长则不受影响。我们初步讨论了 RF2 和 S7 中的 K12 特异性突变是如何发生的，以及为什么 rpsG 处翻译终止效率降低会抑制生长。Schaub 和 Hayes 的工作说明了这样一个事实，由于大肠杆菌 K12 在实验室中的悠久历史，它积累了一些突变，这些突变有时会限制其作为研究原核基因表达基本步骤的模型的价值。
