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首页> 外文期刊>BMC Molecular Biology >Elongation factor eEF1B modulates functions of the release factors eRF1 and eRF3 and the efficiency of translation termination in yeast
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Elongation factor eEF1B modulates functions of the release factors eRF1 and eRF3 and the efficiency of translation termination in yeast

机译:延伸因子eEF1B调节酵母中释放因子eRF1和eRF3的功能以及翻译终止的效率

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Background Termination of translation in eukaryotes is controlled by two interacting polypeptide chain release factors, eRF1 and eRF3. While eRF1 recognizes nonsense codons, eRF3 facilitates polypeptide chain release from the ribosome in a GTP-dependent manner. Besides termination, both release factors have essential, but poorly characterized functions outside of translation.Results To characterize further the functions of yeast eRF1 and eRF3, a genetic screen for their novel partner proteins was performed. As a result, the genes for γ (TEF4 and TEF3/CAM1) and α (TEF5/EFB1) subunits of the translation elongation factor eEF1B, known to catalyze the exchange of bound GDP for GTP on eEF1A, were revealed. These genes act as dosage suppressors of a synthetic growth defect caused by some mutations in the SUP45 and SUP35 genes encoding eRF1 and eRF3, respectively. Extra copies of TEF5 and TEF3 can also suppress the temperature sensitivity of some sup45 and sup35 mutants and reduce nonsense codon readthrough caused by these omnipotent suppressors. Besides, overproduction of eEF1Bα reduces nonsense codon readthrough in the strain carrying suppressor tRNA. Such effects were not shown for extra copies of TEF2, which encodes eEF1A, thus indicating that they were not due to eEF1A activation.Conclusion The data obtained demonstrate involvement of the translation elongation factor eEF1B in modulating the functions of translation termination factors and suggest its possible role in GDP for GTP exchange on eRF3.
机译:背景真核生物中翻译的终止受两个相互作用的多肽链释放因子eRF1和eRF3的控制。尽管eRF1识别无义密码子,但eRF3却以GTP依赖性方式促进多肽链从核糖体释放。除终止外,这两种释放因子在翻译之外均具有重要但功能较弱的功能。结果为了进一步表征酵母eRF1和eRF3的功能,对其新型伴侣蛋白进行了遗传筛选。结果,揭示了翻译延伸因子eEF1B的γ(TEF4和TEF3 / CAM1)和α(TEF5 / EFB1)亚基的基因,这些基因可催化结合的GDP交换eEF1A上的GTP。这些基因充当合成生长缺陷的剂量抑制剂,该合成生长缺陷由分别编码eRF1和eRF3的SUP45和SUP35基因中的某些突变引起。 TEF5和TEF3的额外副本还可以抑制某些sup45和sup35突变体的温度敏感性,并减少由这些全能抑制剂引起的无意义密码子通读。此外,eEF1Bα的过量生产会降低携带抑制性tRNA的菌株中的无义密码子通读。对于编码eEF1A的TEF2的额外拷贝未显示出这种作用,因此表明它们不是由于eEF1A激活所致。结论获得的数据表明翻译延伸因子eEF1B参与调节翻译终止因子的功能,并暗示了其可能的作用。 eRF3上GTP交换在GDP中的作用。

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