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[源自RP1的质粒pRP3.1ts12的缺失导致大肠杆菌K-12中热敏ts12突变的抑制和黏液样表型诱导]

[Deletions of plasmid pRP3.1ts12 derived from RP1 leading to the suppression of the thermosensitive ts12 mutation and mucoid phenotype induction in Escherichia coli K-12].

作者信息

Danilevich V N, Amosenko F A, Shtannikov A V, Kostiuchenko D A

出版信息

Genetika. 1984 Mar;20(3):373-81.

PMID:6370789
Abstract

Properties of a temperature-sensitive in replication mutant pRP3.1ts12 derived from the broad host range RP1 plasmid have been studied. pRP3.1ts12 is a shortened variant of the temperature-sensitive RP1ts12 mutant carrying a deletion in a region from 2.3 to 7.6 MD. In contrast to RP1ts12, the plasmid pRP3.1ts12 is a leaky ts mutant and is characterized by an elevated frequency of reversions to the temperature-independent phenotype. Temperature-independent derivatives of pRP3.1ts12 were studied. Approx. 15% of these were found to induce mucoid growth of the host cells. As revealed from restriction endonuclease analysis, most of the latter derivatives contain deletions of small DNA segments in the region 0.56 to 2.3 MD of the RP1 map. The possible nature of the gene(s), whose deletions suppress the temperature-sensitive ts12 mutation and results in superproduction of Escherichia coli capsular poly-saccharide is discussed.

摘要

对源自广宿主范围RP1质粒的温度敏感复制突变体pRP3.1ts12的特性进行了研究。pRP3.1ts12是温度敏感型RP1ts12突变体的缩短变体,在2.3至7.6 MD区域存在缺失。与RP1ts12不同,质粒pRP3.1ts12是渗漏型温度敏感突变体,其特征是回复到温度非依赖表型的频率升高。对pRP3.1ts12的温度非依赖衍生物进行了研究。发现其中约15%会诱导宿主细胞出现黏液状生长。从限制性内切酶分析可知,大多数后一种衍生物在RP1图谱的0.56至2.3 MD区域含有小DNA片段的缺失。讨论了其缺失抑制温度敏感ts12突变并导致大肠杆菌荚膜多糖超量产生的基因的可能性质。

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