Salmonella typhimurium prfA mutants defective in release factor 1.

Salmonella typhimurium prfA mutants defective in release factor 1.
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鼠伤寒沙门氏菌 prfA 突变体释放因子 1 有缺陷。

DOI:
10.1128/jb.173.13.4144-4154.1991
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发表时间:
1991
影响因子:
3.2
通讯作者:
Wang,X
Wang,X
中科院分区:
生物学3区
文献类型:
--
作者:
Elliott,T;Wang,X

文献摘要

相似文献

鼠伤寒沙门氏菌 prfA 基因中的突变已被定性。这些弱琥珀抑制子显示 UAG 密码子的通读性增加,但 UAA 或 UGA 密码子的通读性没有增加。由于 prfA 上的转录极性,一些 hemA 突变体表现出类似的抑制活性。 prfA 中映射的所有抑制子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,并测定了它们的 DNA 序列。设计了一种方法,通过大肠杆菌recD菌株将测序的突变等位基因转移回其在鼠伤寒沙门氏菌中的原始位置,该菌株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。该重建实验表明,测序的突变足以赋予抑制表型。
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.