SUPPRESSION OF A COLD-SENSITIVE MUTATION IN 16S RIBOSOMAL-RNA BY OVEREXPRESSION OF A NOVEL RIBOSOME-BINDING FACTOR, RBFA
SUPPRESSION OF A COLD-SENSITIVE MUTATION IN 16S RIBOSOMAL-RNA BY OVEREXPRESSION OF A NOVEL RIBOSOME-BINDING FACTOR, RBFA
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DOI：
10.1101/gad.9.5.626
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发表时间：
1995-03-01
影响因子：
10.5
通讯作者：
NOLLER, HF
中科院分区：
文献类型：
--
作者：
DAMMEL, CS;NOLLER, HF
一种新的15-kD蛋白，RbfA，已被确定凭借其作为一个高拷贝抑制剂的能力，以前的特点是显性冷敏感突变（C23 U）在16S rRNA。RbfA被发现与游离的30S核糖体亚基相关，但不与70S核糖体或多聚核糖体相关，并且对于最大细胞生长是必需的，特别是在低温下。在野生型rRNA背景中缺乏RbfA的细胞表现出与冷敏感C23U rRNA突变体惊人相似的冷敏感表型。在含有RbfA敲除结合各种16S rRNA突变的细胞中观察到的等位基因特异性抑制和合成致死性模式表明，RbfA与16S rRNA的5 '末端螺旋区域相互作用，可能在30S成熟的后期步骤期间。
A novel 15-kD 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.