Amemura J, Ichikawa H, Ohtsubo E
Institute of Applied Microbiology, University of Tokyo, Japan.
Gene. 1990 Mar 30;88(1):21-4. doi: 10.1016/0378-1119(90)90055-v.
A series of mutant terminal inverted repeats (IRs), having 2 bp substitutions at various sites within the 38-bp IR sequence of the ampicillin-resistance transposon Tn3, were tested for transposition immunity to Tn3. Mutations within region 1-10 in the IR did not affect transposition immunity, while mutations within region 13-38 inactivated the immunity function. These two regions corresponded to domain A which was not bound specifically by Tn3 transposase and to domain B which was bound by the transposase, respectively. This indicates that specific binding of transposase to domain B within the IR sequence is responsible for transposition immunity.
对一系列突变的末端反向重复序列(IRs)进行了测试,这些序列在氨苄青霉素抗性转座子Tn3的38bp IR序列内的不同位点有2bp的替换,以检测其对Tn3的转座免疫性。IR中1-10区域内的突变不影响转座免疫性,而13-38区域内的突变则使免疫功能失活。这两个区域分别对应于不被Tn3转座酶特异性结合的结构域A和被转座酶结合的结构域B。这表明转座酶与IR序列内结构域B的特异性结合是转座免疫的原因。