Reif H J, Saedler H
Mol Gen Genet. 1975;137(1):17-28. doi: 10.1007/BF00332538.
The DNA sequence IS1, which is 800 pairs long, has been shown to integrate into various bacterial and phage operons. The presence of this DNA sequence in the gal operon of E. coli K12 leads to an 30-2000 fold increase in deletion formation in the gal region as compared to wildtype. This high frequency of deletion formation is specific for IS1 and is independent of the cellular recA function. While the frequency of reversion of gal::IS1 mutations, which also is independent of recA, is not affected by the growth temperature of the cells, the formation of deletions in the gal::IS1 system is strongly dependent on the temperature of growth. Mapping experiments showed that one endpoint of the deletions in most cases is at the site of the IS1 mutation and the second endpoint seems to be at various but preferred sites. The formation of the different classes of delections observed is affected differently by the growth temperature of the cells. A model to account for these results is presented.
长度为800对碱基的DNA序列IS1已被证明可整合到各种细菌和噬菌体操纵子中。与野生型相比，大肠杆菌K12的gal操纵子中存在该DNA序列会导致gal区域缺失形成增加30至2000倍。这种高频率的缺失形成是IS1特有的，并且与细胞recA功能无关。虽然gal::IS1突变的回复频率（同样与recA无关）不受细胞生长温度的影响，但gal::IS1系统中缺失的形成强烈依赖于生长温度。定位实验表明，在大多数情况下，缺失的一个端点位于IS1突变位点，第二个端点似乎位于不同但偏好的位点。观察到的不同类型缺失的形成受细胞生长温度的影响不同。本文提出了一个解释这些结果的模型。
