The Phenomenon of the Uvr+ Dependent Mutagenesis in Salmonella typhimurium
Višnja Bačun-Družina, Jasna Franekić, Marija Alačević, Zdenka Matijašević*
Laboratory of Biology and Microbial Genetics, Faculty of Food Technology and Biotechnology, University of Zagreb, 41000 Zagreb, Pierottieva 6, CROATIA
*Dept. of Pharmacology, University of Massachusetts, Medical School, Worcester, MA 01655, USA
Received October 13, 1994
Accepted February 28, 1995
The Salmonella typhimurium phenotype is comparable to the Escherichia coli ada mutant in having a low but significant constilutively expressed cellular activity of enzyme O6-methyl-guanine DNA-methyltransferase II (MT II) for repair of promutagen lesions O6-methylguanine and O4-methylthymine in DNA. The role of nucleotide excision repair in the mutagenicity of the monofunctional alkylating agents N-methyl-N'-nitro N-nitrosoguanidine (MNNG), methyl methanesulfonate (MMS), N-ethyl-N'-nitro-N-nitrosoguanidine (ENNC), N-ethyl-N-nitro>-sourea (ENU), N-propyl-N'-nitro-N-nitrosoguanidine (PNNG) and N-butyl-N'-nitro-N-nitrosoguanidine (BNNG) in S. typhimurium was examined. Comparing the S. typhimurium uvrB mutant with the nucleotide excision repair proficient strain it has been noticed thai the latter is mutagenized more efficiently at low doses and less efficiently at high doses of methylating (MMS, MNNG) or ethylating (ENU, ENNG) agents. No uvr+ dependent mutagenesis has been noticed in S. typhimurium after treatment by propylating (PNNG) and butylating (BNNG) agents. Our results suggest thai the uvr+ dependent mutagenesis is probably a consequence of the specific competition between enzyme activity involved in nucleotide excision repair enzymes and MT II which are responsible for the overall mutagenic effects of low doses of methylaling and ethylating agent in S. typhimurium.
Presented at the 2nd Croatian Congress of Food Technologists, Biotechnologists and Nutritionists, Zagreb, June15-17,1994