Ahmed A
J Mol Biol. 1984 Mar 15;173(4):523-9. doi: 10.1016/0022-2836(84)90395-4.
Tn9, like other transposable elements, promotes formation of deletions. This activity has been monitored using a plasmid (pAA3B101) on which deletions can be selected positively as galactose-resistant colonies. Measurements of deletion formation by a series of internal deletions of Tn9, generated by restriction endonucleases, show that the two IS1 elements of Tn9 are functionally non-equivalent. IS1-L is active while IS1-R is inactive. The inactive IS1-R element can, however, be reactivated by a deletion which specifically removes the cat promoter. This result indicates that the inactivity of IS1-R is not due to an altered sequence (Galas & Chandler, 1982), but due to inhibition by transcription from the cat promoter (Machida et al., 1983) which acts in a direction opposite to IS1-R transcription. The occurrence of non-equivalent IS in all transposons analysed suggests that this may be an important feature of organization required for the stability of these composite elements.
与其他转座元件一样，Tn9会促进缺失的形成。这种活性已通过一种质粒（pAA3B101）进行监测，在该质粒上，缺失可作为抗半乳糖菌落被正向选择。通过限制性内切酶产生的一系列Tn9内部缺失来测量缺失形成，结果表明Tn9的两个IS1元件在功能上是不等同的。IS1-L是活跃的，而IS1-R是不活跃的。然而，不活跃的IS1-R元件可通过特异性去除cat启动子的缺失而重新激活。这一结果表明，IS1-R的不活跃并非由于序列改变（加拉斯和钱德勒，1982年），而是由于cat启动子的转录抑制（町田等人，1983年），其作用方向与IS1-R转录相反。在所有分析的转座子中都出现了不等同的IS，这表明这可能是这些复合元件稳定性所需的组织的一个重要特征。
