Ligozzi M, Pittaluga F, Fontana R
Institute of Microbiology, University of Verona, Italy.
J Bacteriol. 1993 Apr;175(7):2046-51. doi: 10.1128/jb.175.7.2046-2051.1993.
Enterococcus hirae ATCC 9790 produces a penicillin-binding protein (PBP5) of low penicillin affinity which under certain conditions can take over the functions of all the other PBPs. The 7.1-kb EcoRI fragment containing the pbp5 gene of this strain and of two mutants, of which one (E. hirae R40) overproduces PBP5 and the other (E. hirae Rev14) does not produce PBP5, was cloned in pUC18 and sequenced. In the 7.1-kb EcoRI fragment cloned from strain ATCC 9790, an open reading frame (psr) potentially encoding a 19-kDa protein was identified 1 kb upstream of the pbp5 gene. An 87-bp deletion in this element was found in the 7.1-kb EcoRI fragment cloned from strains R40 and Rev14. In addition, several base substitutions were found in the pbp5 genes of strains R40 and Rev14. One of these converted the 42nd codon, TCA, to the stop codon, TAA, in the pbp5 gene of Rev14. Escherichia coli strains were transformed with plasmids carrying the 7.1-kb EcoRI insert or a 2.6-kb HincII insert containing only the pbp5 gene of the three strains. Immunoblotting analysis of proteins expressed by these transformants showed that the 87-bp deletion in psr was associated with the PBP5 overproducer phenotype of strain R40 and the conversion of the TCA codon to the stop codon was associated with the PBP5 nonproducer phenotype of strain Rev14. None of the other nucleotide substitutions had any apparent effect on the level of PBP5 synthesized.
平肠球菌ATCC 9790产生一种青霉素亲和力低的青霉素结合蛋白(PBP5),在某些条件下,它可以承担所有其他PBP的功能。包含该菌株以及两个突变体pbp5基因的7.1-kb EcoRI片段被克隆到pUC18中并进行测序,其中一个突变体(平肠球菌R40)过量产生PBP5,另一个(平肠球菌Rev14)不产生PBP5。在从菌株ATCC 9790克隆的7.1-kb EcoRI片段中,在pbp5基因上游1 kb处鉴定出一个可能编码19-kDa蛋白的开放阅读框(psr)。在从菌株R40和Rev14克隆的7.1-kb EcoRI片段中发现该元件中有一个87-bp的缺失。此外,在菌株R40和Rev14的pbp5基因中发现了几个碱基替换。其中一个将Rev14的pbp5基因中的第42个密码子TCA转换为终止密码子TAA。用携带7.1-kb EcoRI插入片段或仅包含这三个菌株pbp5基因的2.6-kb HincII插入片段的质粒转化大肠杆菌菌株。对这些转化体表达的蛋白质进行免疫印迹分析表明,psr中的87-bp缺失与菌株R40的PBP5过量生产表型相关,TCA密码子向终止密码子的转换与菌株Rev14的PBP5不生产表型相关。其他核苷酸替换均未对合成的PBP5水平产生任何明显影响。