Mannarelli B M, Lacks S A
J Bacteriol. 1984 Dec;160(3):867-73. doi: 10.1128/jb.160.3.867-873.1984.
When a DNA fragment containing a marker gene was ligated to random chromosomal fragments of Streptococcus pneumoniae and used to transform a recipient strain lacking that gene, the gene was integrated at various locations in the chromosome. Such ectopic integration was demonstrated for the malM gene, and its molecular basis was analyzed with defined donor molecules consisting of ligated fragments containing the malM and sul genes of S. pneumoniae. In a recipient strain deleted in the mal region of its chromosome, these constructs gave Mal+ transformants in which the malM and sul genes were now linked, with malM located between duplicate sul segments. Ectopic integration was unstable under nonselective conditions; mal(sul) ectopic insertions were lost at a rate of 0.05% per generation. Several possible mechanisms of ectopic integration were examined. The donor molecule is most likely to be a circular form of ligated homologous and nonhomologous fragments that, after entry into the cell, undergoes circular synapsis with the recipient chromosome at the site of homology, followed by repair and additive integration.
当一个含有标记基因的DNA片段与肺炎链球菌的随机染色体片段连接,并用于转化缺乏该基因的受体菌株时,该基因整合到了染色体的不同位置。已证实malM基因存在这种异位整合现象,并使用由连接了肺炎链球菌malM和sul基因的片段组成的特定供体分子对其分子基础进行了分析。在其染色体mal区域缺失的受体菌株中,这些构建体产生了Mal+转化体,其中malM和sul基因现在相连,malM位于重复的sul片段之间。在非选择性条件下,异位整合不稳定;mal(sul)异位插入以每代0.05%的速率丢失。研究了几种可能的异位整合机制。供体分子很可能是连接的同源和非同源片段的环状形式,进入细胞后,在同源位点与受体染色体发生环状联会,随后进行修复和附加整合。