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.