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淋病奈瑟菌对氨苄西林自发耐药性的遗传分析。

Genetic analysis of spontaneous resistance to ampicillin in Neisseria gonorrhoeae.

作者信息

Jones F, Cunningham E J, Shockley T E, Jackson J H

出版信息

Antimicrob Agents Chemother. 1985 Jul;28(1):21-7. doi: 10.1128/AAC.28.1.21.

DOI:10.1128/AAC.28.1.21
PMID:3929678
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC176302/
Abstract

Step-wise intrinsic resistance to ampicillin in Neisseria gonorrhoeae was analyzed genetically by DNA-mediated transformation experiments. A first-step ampicillin-resistant (Ampr1) mutant and a second-step ampicillin-resistant (Ampr2) mutant generated during sequential selection were used in these studies. Each selection step was accompanied by an approximate twofold increase in resistance. Four amp alleles were found to account for full resistance of the Ampr2 phenotype. All four amp alleles lie among a cluster of genes which code for ribosomal functions. This region has the map order rif str fus tet cam. First-step resistance was caused by two amp alleles, ampA2 and ampB1, neither of which independently caused detectable ampicillin resistance. Outcrossing of the ampA2 or the ampB1 mutation resulted in wild-type susceptibility to ampicillin. Mapping studies indicate that ampB1 lies between str and fus, whereas ampA2 lies to the right of cam. Second-step resistance required two mutations, ampC3 and ampD4, in addition to ampB1 and ampA2. Transformation of ampC3 to ampC3+ in an Ampr2 mutant resulted in the Ampr1 phenotype. Both ampC3 and ampD4 showed transformation linkage to rif and str. ampC3 was positioned at a site between rif and str. ampD4 apparently occupied a site, outside of the rif-str region, proximal to rif and distal to str. We postulate the gene order to be ampD rif ampC str ampB fus tet cam ampA.

摘要

通过DNA介导的转化实验,对淋病奈瑟菌中逐步产生的氨苄西林内在抗性进行了遗传学分析。在这些研究中使用了在连续选择过程中产生的第一步氨苄西林抗性(Ampr1)突变体和第二步氨苄西林抗性(Ampr2)突变体。每个选择步骤伴随着抗性大约两倍的增加。发现四个amp等位基因导致了Ampr2表型的完全抗性。所有四个amp等位基因都位于一组编码核糖体功能的基因簇中。该区域的图谱顺序为rif str fus tet cam。第一步抗性由两个amp等位基因ampA2和ampB1引起,它们单独都不会导致可检测到的氨苄西林抗性。ampA2或ampB1突变的异型杂交导致对氨苄西林的野生型敏感性。图谱研究表明,ampB1位于str和fus之间,而ampA2位于cam的右侧。除了ampB1和ampA2之外,第二步抗性还需要两个突变ampC3和ampD4。在Ampr2突变体中将ampC3转化为ampC3 +会导致Ampr1表型。ampC3和ampD4都显示出与rif和str的转化连锁。ampC3位于rif和str之间的位点。ampD4显然占据了rif-str区域之外、靠近rif且远离str的一个位点。我们推测基因顺序为ampD rif ampC str ampB fus tet cam ampA。

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