ogt alkyltransferase enhances dibromoalkane mutagenicity in excision repair-deficient Escherichia coli K-12.
Affiliation
Departamento de Genética, Facultad de Ciencias, Universidad de Córdoba, Espana.Issue Date
1995-02
Metadata
Show full item recordAbstract
We examined the role of the O6-alkylguanine-DNA alkyltransferase encoded by ogt gene in the sensitivity of Escherichia coli to the mutagenic effects of the dibromoalkanes, dibromoethane and dibromomethane, by comparing responses in ogt- bacteria to those in their isogenic ogt+ parental counterparts. The effects of the uvrABC excision-repair system, the adaptive response, mucAB and umuDC mutagenic processing, and glutathione bioactivation on the differential responses of ogt- and ogt+ bacteria were also studied. Mutation induction was monitored by measuring the frequency of forward mutations to L-arabinose resistance. Induced mutations occurred only in excision repair-defective strains and were totally (with dibromomethane) or substantially (with dibromoethane) dependent on the alkyltransferase (ATase) encoded by the ogt gene. An increased mutagenic response to both dibromoalkanes was also seen in ogt- bacteria that overexpressed the ogt protein from a multicopy plasmid, indicating that the differences in mutability between ogt+ and ogt- bacteria were not dependent on the ogt- null allele carried by the defective strain. The ATase encoded by the constitutive ogt gene was more effective in promoting dibromoalkane mutagenicity than the ada ATase induced by exposure to low doses of a methylating agent. The mutagenicity promoted by the ogt ATase was dependent on both glutathione bioactivation and SOS mutagenic processing. To our knowledge, this paper presents for the first time evidence that DNA ATases, in particular the ATase encoded by the ogt gene, can increase the mutagenic effects of a DNA-damaging agent. The mechanism of this effect has yet to be established.Citation
ogt alkyltransferase enhances dibromoalkane mutagenicity in excision repair-deficient Escherichia coli K-12. 1995, 12 (2):110-7 Mol. Carcinog.Journal
Molecular CarcinogenesisDOI
10.1002/mc.2940120208PubMed ID
7662116Type
ArticleLanguage
enISSN
0899-1987ae974a485f413a2113503eed53cd6c53
10.1002/mc.2940120208
Scopus Count
Collections
Related articles
- Bacterial and mammalian DNA alkyltransferases sensitize Escherichia coli to the lethal and mutagenic effects of dibromoalkanes.
- Authors: Abril N, Luque-Romero FL, Prieto-Alamo MJ, Rafferty JA, Margison GP, Pueyo C
- Issue date: 1997 Oct
- Mutagenesis and DNA repair for alkylation damages in Escherichia coli K-12.
- Authors: Abril N, Roldán-Arjona T, Prieto-Alamo MJ, van Zeeland AA, Pueyo C
- Issue date: 1992
- Mammalian cells expressing Escherichia coli O6-alkylguanine-DNA alkyltransferases are hypersensitive to dibromoalkanes.
- Authors: Abril N, Margison GP
- Issue date: 1999 Jun
- Role of DNA repair by (A)BC excinuclease and Ogt alkyltransferase in the final distribution of LacI-d mutations induced by N-butyl-N-nitrosourea in Escherichia coli.
- Authors: Ferrezuelo F, Prieto-Alamo MJ, Jurado J, Pueyo C
- Issue date: 1998 Sep
- Influence of DNA repair by (A)BC excinuclease and Ogt alkyltransferase on the distribution of mutations induced by n-propyl-N-nitrosourea in Escherichia coli.
- Authors: Ferrezuelo F, Prieto-Alamo MJ, Jurado J, Pueyo C
- Issue date: 1998