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鼠伤寒沙门氏菌的aroA和serC基因构成一个操纵子。

Genes aroA and serC of Salmonella typhimurium constitute an operon.

作者信息

Hoiseth S K, Stocker B A

出版信息

J Bacteriol. 1985 Jul;163(1):355-61. doi: 10.1128/jb.163.1.355-361.1985.

Abstract

Genetic analysis of aroA554::Tn10 derivatives of two mouse-virulent Salmonella typhimurium strains, "FIRN" and "WRAY," and of a nonreverting derivative of each constructed for use as a live vaccine, showed the site of the insertion among mapped aroA point mutants. The WRAY live-vaccine strain gave no aro+ recombinants in crosses with aroA point mutations to one side of the insertion, indicating a deletion from Tn10 through the sites of these point mutations. The FIRN live-vaccine strain gave wild-type recombinants with all tested point mutants; it probably has a deletion or inversion extending from Tn10 into aroA but not as far as the nearest point mutation. Some tetracycline-sensitive mutants of aroA554::Tn10 strains required serine and pyridoxine, indicating loss of serC function, and some that were found to be SerC- did not produce gas from glucose, indicating a loss of pfl function. These results show the gene order pfl-serC-aroA, as in Escherichia coli. Ampicillin enrichment applied to pools of tetracycline-sensitive mutants of strains with Tn10 insertions near aroA (i.e., zbj::Tn10 strains) yielded Aro- SerC- Pfl-, Aro- SerC+ Pfl+, and Aro- SerC- Pfl+ mutants but none which were Aro+ SerC-. All of the mutants are explicable by deletions or inversions extending clockwise from zbj::Tn10 into or through an operon comprising serC (promoter-proximal) and aroA. Such an operon was also shown by the identification of two Tn10 insertions causing phenotype Aro- SerC-, each able to revert to Aro+ SerC+ by precise excision. serC corresponds to the open reading frame promoter-proximal to aroA that was identified elsewhere by base sequencing of a cloned aroA segment of S. typhimurium (Comai et al., Science 221:370-371, 1983). Both serine and chorismate are precursors of enterochelin; this may be why serC and aroA are in a single operon.

摘要

对两株鼠伤寒沙门氏菌强毒株“FIRN”和“WRAY”的aroA554::Tn10衍生物以及为用作活疫苗构建的各株非回复性衍生物进行遗传分析,确定了插入位点在已定位的aroA点突变体中的位置。WRAY活疫苗株与插入位点一侧的aroA点突变体杂交时未产生aro+重组体,表明从Tn10到这些点突变位点发生了缺失。FIRN活疫苗株与所有测试的点突变体均产生野生型重组体;它可能有一个从Tn10延伸到aroA的缺失或倒位,但未延伸到最近的点突变处。aroA554::Tn10菌株的一些四环素敏感突变体需要丝氨酸和吡哆醇,表明serC功能丧失,一些被发现为SerC-的突变体不能利用葡萄糖产气,表明pfl功能丧失。这些结果表明基因顺序为pfl-serC-aroA,与大肠杆菌中的情况相同。对aroA附近有Tn10插入的菌株(即zbj::Tn10菌株)的四环素敏感突变体库进行氨苄青霉素富集,得到了Aro-SerC-Pfl-、Aro-SerC+Pfl+和Aro-SerC-Pfl+突变体,但没有Aro+SerC-突变体。所有这些突变体都可以通过从zbj::Tn10顺时针延伸到或穿过一个包含serC(启动子近端)和aroA的操纵子的缺失或倒位来解释。通过鉴定两个导致Aro-SerC-表型的Tn10插入也证明了这样一个操纵子,每个插入都能够通过精确切除回复为Aro+SerC+。serC对应于鼠伤寒沙门氏菌aroA启动子近端的开放阅读框,这在其他地方通过对克隆的aroA片段进行碱基测序得以确定(科马伊等人,《科学》221:370 - 371,1983)。丝氨酸和分支酸都是肠螯合素的前体;这可能就是serC和aroA存在于一个操纵子中的原因。

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