Hughes D, Atkins J F, Thompson S
Department of Genetics, Trinity College, Dublin Ireland.
EMBO J. 1987 Dec 20;6(13):4235-9. doi: 10.1002/j.1460-2075.1987.tb02772.x.
This is the first report of ribosomal frameshifting promoted by mutants of the elongation factor Tu (EF-Tu). EF-Tu mutants can suppress both -1 and +1 frameshift mutations. The level of nonsense readthrough is also increased at some UGA (this paper) and UAG (Hughes, 1987) sites by these mutants. Suppression occurs when a mutant tuf allele is paired with a wild-type copy of the other tuf gene but is most efficient when both tuf genes are mutant. Frameshifting mediated by the tuf alleles studied, tufA8 and tufB103, is not general; indeed most frameshift mutations are not suppressed. Several possible mechanisms by which mutant EF-Tu may cause frameshifting are discussed.
这是关于延伸因子Tu(EF-Tu)突变体促进核糖体移码的首次报道。EF-Tu突变体能够抑制 -1和 +1移码突变。这些突变体还会使一些UGA(本文)和UAG(休斯,1987年)位点的无义通读水平升高。当一个突变的tuf等位基因与另一个tuf基因的野生型拷贝配对时会发生抑制作用,但当两个tuf基因均为突变型时抑制效率最高。所研究的tuf等位基因tufA8和tufB103介导的移码并不普遍;实际上,大多数移码突变并未被抑制。文中讨论了突变型EF-Tu可能导致移码的几种可能机制。