Tanaka M, Matsushita K, Yamamoto T
Antimicrob Agents Chemother. 1985 Aug;28(2):227-34. doi: 10.1128/AAC.28.2.227.
Plasmid R753-1-encoded resistance to ampicillin (by production of OXA-1 [type II] beta-lactamase), streptomycin, and sulfonamide was analyzed functionally and physically. The OXA-1 beta-lactamase gene on R753-1 could not transpose, whereas on some plasmids this gene was capable of transposition as part of transposon Tn2603. By using the nontransposable gene on R753-1 with Tn21 on a separate plasmid, we observed the genesis of a complex transposon with a structure similar to that of Tn2603. This finding confirms our previous hypothesis that Tn2603 has evolved directly from Tn21 through acquisition of the OXA-1 beta-lactamase gene by substitution of DNA segments. Furthermore, the mechanism of mobilization of pACYC184 derivatives by RecA-dependent homologous recombination was demonstrated.
对质粒R753 - 1编码的对氨苄青霉素(通过产生OXA - 1[II型]β - 内酰胺酶)、链霉素和磺胺的抗性进行了功能和物理分析。R753 - 1上的OXA - 1β - 内酰胺酶基因不能转座,而在一些质粒上,该基因作为转座子Tn2603的一部分能够转座。通过在一个单独的质粒上使用R753 - 1上的不可转座基因和Tn21,我们观察到了一个结构与Tn2603相似的复合转座子的产生。这一发现证实了我们之前的假设,即Tn2603是通过DNA片段替换获得OXA - 1β - 内酰胺酶基因而直接从Tn21进化而来的。此外,还证明了RecA依赖的同源重组对pACYC184衍生物的动员机制。