IS10在低频情况下促进相邻缺失。
IS10 promotes adjacent deletions at low frequency.
作者信息
Roberts D E, Ascherman D, Kleckner N
机构信息
Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, Massachusetts 02138.
出版信息
Genetics. 1991 May;128(1):37-43. doi: 10.1093/genetics/128.1.37.
Some transposable elements move by a replicative mechanism involving cointegrate formation. Intramolecular cointegration can generate a product called an "adjacent deletion" in which a contiguous chromosomal segment adjacent to the transposon is deleted while the element responsible remains intact. Insertion sequence IS10 is thought to transpose by a nonreplicative mechanism. In the simplest models, nonreplicative transposition cannot give rise to an adjacent deletion because an intrinsic feature of such transposition is excision of the IS element from the donor location. We report here that IS10 can generate adjacent deletions, but at a frequency which is approximately 1/30th the frequency of transposition for the same element. We suggest that these deletions might arise either by nonreplicative transposition events that involve two IS10 elements located on sister chromosomes or by aberrant nonreplicative events involving cleavage and ligation at only one end of the element.
一些转座元件通过涉及共整合体形成的复制机制移动。分子内共整合可产生一种称为“相邻缺失”的产物，其中转座子相邻的连续染色体片段被删除，而负责的元件保持完整。插入序列IS10被认为通过非复制机制转座。在最简单的模型中，非复制转座不会导致相邻缺失，因为这种转座的一个内在特征是IS元件从供体位置切除。我们在此报告，IS10可产生相邻缺失，但其频率约为同一元件转座频率的1/30。我们认为这些缺失可能是由涉及位于姐妹染色体上的两个IS10元件的非复制转座事件引起的，或者是由仅涉及元件一端的切割和连接的异常非复制事件引起的。
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