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~Y~/~rch, 2~9 (I~93) 193-2~ © 1£~3 El:~-der S~e~.:~ l~]~rs B.V. Atl r~t~ re~r,'ed 016~-121S/93/$~.C0 MUTGEN Multiple pathways of deletion formation in EschePichia coli Elias Balbinder Department of Biochemistry, Biophysics and Genetics and Colorado Cancer Center, Un&,ersity of Colorado Health Sciences Center, 4200 East 9th Avenue, P.O. Box B 121, Denver, CO 80262, USA (Received 24 June 1992) (Revision received 29 December 1992) (Accepted 11 January 1993) 193 Keywords: Deletions; Palindromes; SOS repair, Tnl0 ~cision; RecBC; Mutant selection for deletion enhancement Summary We are investigating the mechanisms for deletion formation through the use of mutants which alter deletion frequency together with well characterized systems for deletion detection. We report here on three mutations which were isolated for their ability to stimulate deletions in plasmid pMC874 (dli mutations). The mutation rec-2251(formerly known as dlil) is a new allele of recBCD, a group of genes coding for the polypeptide components of the major recombination enzyme complex in E. coli; the second one, dli2 may be a new allele of uorD, which codes for DNA heliease II; and the third one, d//3, has the phenotype of a mismatch repair mutation. Here we compare the effeets of mutations in SOS-repair genes to those of the dli mutations on three different deletion events: (a) the deletion of short (60-100-bp) palindromic and non-palindromic inserts in derivatives of plasmid pBR325; (b) larger (600-800-bp) deletions in plasmid pMC874; and (e) the excision of the Tnl0 transposon from chromoso- mal sites. Our results indicate that some form of SOS processing stimulates the loss of palindromes but not non-palindromes in plasmid pBR325 derivatives, and that RecA is necessary for UV-induced excision of Tnl0 but this event is inhibited by UmuCD or its homolog MucAB. Each of the dli mutations showed unique effects on different classes of deletions. Mutation rec-2251 stimulated specifically deletions in pMC874 but had no effect on the deletion of non-palindromes in pBP,325, and reduced the incidence of the other del6tion events tested including loss.of palindromic inserts in pBR325 as well as Tnl0 excision. Mutation dli2, on the other hand, stimulated all deletions tested to varying extents, while dli3 did not affect markedly deletion formation in pBR325 plasmids but had a large stimulatory effect on both deletions in plasmid pMC874 and Tnl0 exeision. These results reveal that (a) some SOS-repair functions participate in deletion formation, (b) mutations selected ~for altering the incidence of one class of deletions may have totally different effects on other deletion events, and (e) the differences in mutant Correspondence: Dr. Elias Balbinder, Department of Bio- chemistry, Biophysics and Genetics and Colorado Cancer Center, Unive~slty of CoIDrado Health Sciences Center, 4200 East 9th Avenue, P.O. B~x B 121, Dem'er, CO 80262, USA. 40000084