鼠伤寒沙门氏菌中释放因子1缺陷的prfA突变体。
Salmonella typhimurium prfA mutants defective in release factor 1.
作者信息
Elliott T, Wang X
机构信息
Department of Microbiology, University of Alabama, Birmingham 35294.
出版信息
J Bacteriol. 1991 Jul;173(13):4144-54. doi: 10.1128/jb.173.13.4144-4154.1991.
Abstract
Mutations have been characterized that map in the prfA gene of Salmonella typhimurium. These weak amber suppressors show increased readthrough of UAG but not UAA or UGA codons. Some hemA mutants exhibit a similar suppressor activity due to transcriptional polarity on prfA. All of the suppressors mapping in prfA are recessive to the wild type. Two mutant prfA genes were cloned onto plasmids, and their DNA sequences were determined. A method was devised for transferring the sequenced mutant alleles back to their original location in S. typhimurium via an Escherichia coli recD strain that carries the entire S. typhimurium hemA-prfA operon as a chromosomal insertion in trp. This reconstruction experiment showed that the mutations sequenced are sufficient to confer the suppressor phenotype.
摘要
已对鼠伤寒沙门氏菌prfA基因中的突变进行了表征。这些弱琥珀抑制子显示UAG密码子的通读增加，但UAA或UGA密码子的通读未增加。一些hemA突变体由于对prfA的转录极性而表现出类似的抑制活性。所有定位在prfA中的抑制子相对于野生型都是隐性的。将两个突变的prfA基因克隆到质粒上，并测定其DNA序列。设计了一种方法，通过携带整个鼠伤寒沙门氏菌hemA-prfA操纵子作为trp中的染色体插入的大肠杆菌recD菌株，将测序的突变等位基因转移回它们在鼠伤寒沙门氏菌中的原始位置。这个重建实验表明，测序的突变足以赋予抑制子表型。
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本文引用的文献
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