大肠杆菌K-12中R质粒R1的β-内酰胺酶缺陷型（bla）突变体的特性分析及其与RP1类似突变体的比较。
Characterization of beta-lactamase-deficient (bla) mutants of the R plasmid R1 in Escherichia coli K-12 and comparison with similar mutants of RP1.
作者信息
Crowlesmith I, Howe T G
出版信息
Antimicrob Agents Chemother. 1980 Nov;18(5):667-74. doi: 10.1128/AAC.18.5.667.
Abstract
Thirty-eight mutants of R1, an R plasmid specifying the type IIIa (TEM) beta-lactamase, were isolated; these mutants are partially or totally unable to synthesize the type IIIa beta-lactamase. The loss of beta-lactamase activity was associated with a reduction in the level of penicillin resistance conferred by the mutants upon their host strain. At least two of the mutants synthesized a beta-lactamase with altered substrate specificity. These properties are compared with those of two beta-lactamase-deficient mutants of plasmid RP1. The results suggest that, for both R plasmids, penicillin resistance is entirely attributable to the presence of beta-lactamase activity. The properties of two R1 derivatives, pUB251 and pUB252, which have phenotypes similar to that of RP1, support this conclusion.
摘要
分离出了38个R1突变体，R1是一种携带IIIa型（TEM）β-内酰胺酶的R质粒；这些突变体部分或完全无法合成IIIa型β-内酰胺酶。β-内酰胺酶活性的丧失与突变体赋予其宿主菌株的青霉素抗性水平降低有关。至少有两个突变体合成了底物特异性改变的β-内酰胺酶。将这些特性与质粒RP1的两个β-内酰胺酶缺陷突变体的特性进行了比较。结果表明，对于这两种R质粒，青霉素抗性完全归因于β-内酰胺酶活性的存在。两个R1衍生物pUB251和pUB252的表型与RP1相似，其特性支持了这一结论。
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