Takasu-Ishikawa E, Yoshihara M, Hotta Y
Department of Physics, Faculty of Science, University of Tokyo, Japan.
Mol Gen Genet. 1992 Mar;232(1):17-23. doi: 10.1007/BF00299132.
We have previously established a transgenic Drosophila line with a highly transposable P element insertion. Using this strain we analyzed transposition and excision of the P element at the molecular level. We examined sequences flanking the new insertion sites and those of the remnants after excision. Our results on mobilization of the P element demonstrate that target-site duplication at the original insertion site does not play a role in forward excision and transposition. After P element excision an 8 bp target-site duplication and part of the 31 bp terminal inverted repeat (5-18 bp) remained in all the strains examined. Moreover, in 11 out of 28 strains, extra sequences were found between the two remaining inverted repeats. The double-strand gap repair model does not explain the origin of these extra sequences. The mechanism creating them may be similar to the hairpin model proposed for the transposon Tam in Antirrhinum majus.
我们先前已建立了一个带有高度可转座P元件插入的转基因果蝇品系。利用该品系，我们在分子水平上分析了P元件的转座和切除。我们检查了新插入位点两侧的序列以及切除后残余物的序列。我们关于P元件移动的结果表明，原始插入位点处的靶位点重复在正向切除和转座中不起作用。在P元件切除后，在所检查的所有品系中都保留了一个8 bp的靶位点重复以及31 bp末端反向重复序列的一部分（5 - 18 bp）。此外，在28个品系中的11个品系中，在两个剩余的反向重复序列之间发现了额外的序列。双链缺口修复模型无法解释这些额外序列的起源。产生它们的机制可能类似于为金鱼草中的转座子Tam提出的发夹模型。
