Moerman D G, Kiff J E, Waterston R H
Department of Zoology, University of British Columbia, Vancouver, Canada.
Nucleic Acids Res. 1991 Oct 25;19(20):5669-72. doi: 10.1093/nar/19.20.5669.
We have examined eight germline revertants generated by the excision of Tc1 from a site within the unc-22 gene of Caenorhabditis elegans. A rich variety of rearrangements accompanied Tc1 excision at this site, including transposon 'footprints', deletions of sequences flanking the insertion site and direct nontandem duplications of flanking DNA. With only modest modification the double-strand gap repair model for transposition, recently proposed by Engles and coworkers (Cell 62: 515-525 1990), can explain even the most complex of these rearrangements. In light of this model rearrangements of the target site accompanying transposition/excision may not be the end result of imprecise excision of the element. Instead, these rearrangements may be the result of imprecise repair of the double-strand gap by the host replication and repair machinery. Sequences surrounding an insertion site influence the fidelity of gap repair by this machinery. This may lead to a number of possible resolutions of a double-strand gap as documented here for a Tc1 site in unc-22.
我们检测了通过从秀丽隐杆线虫unc-22基因内的一个位点切除Tc1而产生的八个种系回复突变体。在该位点,伴随着Tc1切除出现了丰富多样的重排,包括转座子“足迹”、插入位点侧翼序列的缺失以及侧翼DNA的直接非串联重复。只需进行适度修改,Engles及其同事最近提出的转座双链缺口修复模型(《细胞》62: 515 - 525, 1990)就能解释这些重排中最为复杂的情况。根据这个模型,伴随转座/切除的靶位点重排可能并非元件不精确切除的最终结果。相反,这些重排可能是宿主复制和修复机制对双链缺口进行不精确修复的结果。插入位点周围的序列会影响该机制对缺口修复的保真度。这可能导致双链缺口出现多种可能的修复结果,就如同这里记录的unc-22基因中一个Tc1位点的情况一样。