Yamashita S, Mikami T, Kishima Y
Laboratory of Genetic Engineering, Faculty of Agriculture, Hokkaido University, Sapporo, Japan.
Mol Gen Genet. 1998 Sep;259(5):468-74. doi: 10.1007/s004380050837.
Most transposon families consist of heterogeneous copies with varying sizes. In contrast, the Tam3 copies in Antirrhinum majus are known to have exceptionally conserved structures of uniform size. Gap repair has been reported to be involved in the structural alteration of copies from several transposon families. In this study, we have asked whether or not gap repair has affected Tam3 copies. Five Tam3 copies carrying aberrant sequences were selected from 40 independent Tam3 clones and their sequences were analyzed. Two of the five copies contain insertions in the Tam3 sequence. These two insertions, designated Tam356 and Tam661, are typical transposon-like sequences, which have terminal inverted repeats and cause target site duplication. These nested transposons were obviously associated with transpositional events, and did not originate from the gap-repair process. The remaining three copies had lost large parts of the Tam3 sequence. We could not find any relationship between the deletions of Tam3 sequence in the three copies and gap repair. PCR analysis of a Tam3 excision site in the nivea(recurrence:Tam3) mutant also showed that most of the repair events after the Tam3 excision involved end-joining. In addition to the results obtained here, among the other clones isolated, we could not find any of the internally deleted copies that comprise a major part of other transposon families. All of these data suggest that some feature of the Tam3 structure suppresses the structural alterations that are otherwise generated during the gap repair process.
大多数转座子家族由大小各异的异质拷贝组成。相比之下,已知金鱼草中的Tam3拷贝具有异常保守且大小一致的结构。据报道,缺口修复参与了几个转座子家族拷贝的结构改变。在本研究中,我们探究了缺口修复是否影响了Tam3拷贝。从40个独立的Tam3克隆中挑选出5个携带异常序列的Tam3拷贝,并对其序列进行了分析。5个拷贝中有2个在Tam3序列中含有插入片段。这两个插入片段,分别命名为Tam356和Tam661,是典型的转座子样序列,具有末端反向重复序列并导致靶位点重复。这些嵌套转座子显然与转座事件相关,并非起源于缺口修复过程。其余3个拷贝缺失了大部分Tam3序列。我们未发现这3个拷贝中Tam3序列的缺失与缺口修复之间存在任何关联。对nivea(复发:Tam3)突变体中一个Tam3切除位点的PCR分析也表明,Tam3切除后的大多数修复事件涉及末端连接。除了此处获得的结果外,在分离出的其他克隆中,我们未发现任何构成其他转座子家族主要部分的内部缺失拷贝。所有这些数据表明,Tam3结构的某些特征抑制了在缺口修复过程中原本会产生的结构改变。