Delattre M, Anxolabéhère D, Coen D
Département Dynamique du Génome et Evolution, Institut Jacques Monod, Paris, France.
Genetics. 1995 Dec;141(4):1407-24. doi: 10.1093/genetics/141.4.1407.
We have studied P transposase-induced events on a P[w] transgene, P[wd1], harboring the whole white gene with a 3.44-kb direct duplication of its 5' regulatory sequences (containing the ZESTE-binding region, ZBR). We have recovered mutations leading to an increase or a decrease of zeste1 repression, generally as the consequence of modifications of number of ZBR in close physical proximity and/or jumps to other sites. We describe mutants displaying deletions of the original duplicated sequence or increases in the number of repeats from two to three or four. Internal deletions are more frequent than amplifications. Both require the integrity of P-element ends. We have also observed a high frequency of double P elements localized at the original P[wd1] insertion site. These double P elements are arranged in nonrandom configurations. We discuss the frequencies and the possible mechanisms leading to the various types of derivatives, in light of the current models for P excision and transposition. We propose that the P transposase induces mainly localized events. Some of these could result from frequent changes of template during gap-repair DNA synthesis, and/or from abortive transposition.
我们研究了P转座酶在携带完整白色基因的P[w]转基因P[wd1]上诱导的事件,该基因带有其5'调控序列(包含ZESTE结合区域,ZBR)的3.44 kb直接重复序列。我们已经获得了导致zeste1抑制增加或减少的突变,通常是由于紧密物理邻近的ZBR数量改变和/或跳跃到其他位点的结果。我们描述了显示原始重复序列缺失或重复次数从两个增加到三个或四个的突变体。内部缺失比扩增更频繁。两者都需要P元件末端的完整性。我们还观察到在原始P[wd1]插入位点处有高频的双P元件。这些双P元件以非随机构型排列。根据当前的P切除和转座模型,我们讨论了导致各种类型衍生物的频率和可能机制。我们提出P转座酶主要诱导局部事件。其中一些可能是由于间隙修复DNA合成过程中模板的频繁变化和/或流产转座导致的。