Samulski R J, Srivastava A, Berns K I, Muzyczka N
Cell. 1983 May;33(1):135-43. doi: 10.1016/0092-8674(83)90342-2.
We have isolated three types of pBR322-AAV recombinant plasmids that contain deletions within the 145 bp AAV terminal repeats. When the plasmids were transfected into human cells, mutants that contained deletions within the left (type I) or right (type II) terminal repeat were viable. Of four mutants examined that contained deletions in both termini (type III), only one was viable. All of the viable mutants produced AAV virions that contained wild-type AAV DNA. Furthermore, the viable type III deletion could be converted to a nonviable mutant by deleting all copies of an 11 bp sequence from its termini. We conclude that there is an efficient mechanism for correcting deletions within the AAV termini. A model that could account for these observations is also discussed.
我们分离出了三种pBR322-AAV重组质粒，它们在145 bp的腺相关病毒（AAV）末端重复序列内存在缺失。当这些质粒转染到人细胞中时，在左末端重复序列（I型）或右末端重复序列（II型）内有缺失的突变体是存活的。在检测的四个在两个末端都有缺失的突变体（III型）中，只有一个是存活的。所有存活的突变体都产生了含有野生型AAV DNA的AAV病毒粒子。此外，通过从其末端删除11 bp序列的所有拷贝，存活的III型缺失可以转化为非存活突变体。我们得出结论，存在一种纠正AAV末端内缺失的有效机制。还讨论了一个可以解释这些观察结果的模型。
