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革兰氏阴性菌中的抗生素耐药性:基因盒与整合子的作用

Antibiotic resistance in gram-negative bacteria: the role of gene cassettes and integrons.

作者信息

Hall R M, Collis C M

机构信息

CSIRO Molecular Science, Sydney Laboratory, New South Wales, Australia.

出版信息

Drug Resist Updat. 1998;1(2):109-19. doi: 10.1016/s1368-7646(98)80026-5.

DOI:10.1016/s1368-7646(98)80026-5
PMID:16904397
Abstract

Resistance of gram-negative organisms to antibiotics such as beta-lactams, aminoglycosides, trimethoprim and chloramphenicol is caused by many different acquired genes, and a substantial proportion of these are part of small mobile elements known as gene cassettes. A gene cassette consists of the gene and a downstream sequence, known as a 59-base element (59-be), that acts as a specific recombination site. Gene cassettes can move into or out of a specific receptor site (attl site) in a companion element called an integron, and integration or excision of the cassettes is catalysed by a site-specific recombinase (Intl) that is encoded by the integron. At present count there are 40 different cassette-associated resistance genes and three distinct classes of integron, each encoding a distinct Intl integrase. The same cassettes are found in all three classes of integron, indicating that cassettes can move freely between different integrons. Integrons belonging to class I often contain a further antibiotic resistance gene, sull, conferring resistance to sulphonamides. The sull gene is found in a conserved region (3'-CS) that is not present in all members of this class. Class I integrons of the sull type are most prevalent in clinical isolates and have been found in many different organisms. Even though most of them are defective transposon derivatives, having lost at least one of the transposition genes, they are none the less translocatable and consequently found in many different locations. The transposon Tn7 is the best known representative of class 2 integrons, and Tn7 and relatives are also found in many different species.

摘要

革兰氏阴性菌对β-内酰胺类、氨基糖苷类、甲氧苄啶和氯霉素等抗生素的耐药性是由许多不同的获得性基因引起的,其中很大一部分是称为基因盒的小型移动元件的一部分。基因盒由基因和一个下游序列组成,该下游序列称为59碱基元件(59-be),作为特定的重组位点。基因盒可以移入或移出称为整合子的伴随元件中的特定受体位点(attl位点),盒的整合或切除由整合子编码的位点特异性重组酶(Intl)催化。目前已发现有40种不同的与盒相关的耐药基因和三类不同的整合子,每类整合子编码一种不同的Intl整合酶。在所有三类整合子中都发现了相同的基因盒,这表明基因盒可以在不同的整合子之间自由移动。I类整合子通常还含有另一个抗生素耐药基因sull,赋予对磺胺类药物的耐药性。sull基因位于一个保守区域(3'-CS)中,并非该类所有成员都有此区域。sull型的I类整合子在临床分离株中最为普遍,并且已在许多不同的生物体中发现。尽管它们中的大多数是有缺陷的转座子衍生物,至少失去了一个转座基因,但它们仍然是可转位的,因此存在于许多不同的位置。转座子Tn7是2类整合子最著名的代表,并且Tn7及其相关转座子也在许多不同的物种中发现。

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