Suppr超能文献

通过一种新型核糖体结合因子RbfA的过表达抑制16S rRNA中的冷敏感突变。

Suppression of a cold-sensitive mutation in 16S rRNA by overexpression of a novel ribosome-binding factor, RbfA.

作者信息

Dammel C S, Noller H F

机构信息

Department of Biology, University of California at Santa Cruz 95064.

出版信息

Genes Dev. 1995 Mar 1;9(5):626-37. doi: 10.1101/gad.9.5.626.

Abstract

A novel 15-kDa protein, RbfA, has been identified by virtue of its ability to act as a high copy suppressor of a previously characterized dominant cold-sensitive mutation (C23U) in 16S rRNA. RbfA is found associated with free 30S ribosomal subunits, but not with 70S ribosomes or polysomes, and is essential for maximal cell growth, particularly at low temperatures. Cells lacking RbfA in a wild-type rRNA background exhibit a cold-sensitive phenotype that is strikingly similar to that of the cold-sensitive C23U rRNA mutant. The observed patterns of allele specificity of suppression and synthetic lethality in cells containing an RbfA knockout in combination with various 16S rRNA mutations suggests that RbfA interacts with the 5'-terminal helix region of 16S rRNA, possibly during a late step of 30S maturation.

摘要

一种新的15 kDa蛋白RbfA已被鉴定出来,这是因为它能够作为先前已鉴定的16S rRNA中显性冷敏感突变(C23U)的高拷贝抑制因子。发现RbfA与游离的30S核糖体亚基相关联,但不与70S核糖体或多核糖体相关联,并且对于最大程度的细胞生长至关重要,尤其是在低温下。在野生型rRNA背景中缺乏RbfA的细胞表现出冷敏感表型,这与冷敏感C23U rRNA突变体的表型惊人地相似。在含有RbfA基因敲除与各种16S rRNA突变组合的细胞中观察到的抑制和合成致死的等位基因特异性模式表明,RbfA可能在30S成熟的后期与16S rRNA的5'-末端螺旋区域相互作用。

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