Balasundaram D, Dinman J D, Tabor C W, Tabor H
Laboratory of Biochemical Pharmacology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892-0830.
J Bacteriol. 1994 Nov;176(22):7126-8. doi: 10.1128/jb.176.22.7126-7128.1994.
We previously showed that a mutant of Saccharomyces cerevisiae, which cannot make spermidine as a result of a deletion in the SPE2 gene (spe2 delta), exhibits a marked elevation in +1 ribosomal frameshifting efficiency in response to the Ty1 frameshift sequence, CUU AGG C. In the present study, we found that spermidine deprivation alone does not result in increased +1 ribosomal frameshifting efficiency. The high level of +1 ribosomal frameshifting efficiency in spe2 delta cells is the result of the combined effects of both spermidine deprivation and the large increase in the level of intracellular putrescine resulting from the derepression of the gene for ornithine decarboxylase (SPE1) in spermidine-deficient strains.
我们之前发现,由于SPE2基因缺失(spe2Δ)而无法合成亚精胺的酿酒酵母突变体,在响应Ty1移码序列CUU AGG C时,+1核糖体移码效率显著提高。在本研究中,我们发现单独的亚精胺缺乏并不会导致+1核糖体移码效率增加。spe2Δ细胞中高水平的+1核糖体移码效率是亚精胺缺乏和亚精胺缺陷菌株中鸟氨酸脱羧酶基因(SPE1)去抑制导致细胞内腐胺水平大幅增加共同作用的结果。