Escherichia coli gene that controls sensitivity to alkylating agents

Yamamoto, Y; Katsuki, Motoya; Sekiguchi, M; Otsuji, Nozomu

doi:10.1128/jb.135.1.144-152.1978

Cited by 80 publications

(20 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…E. coli strains used in this work are listed in Table 1. Strain MS23 is his' alkA and cogenic with AB1157 except for the his-alkA region (53). hisG hisD+ derivatives were constructed by transducing AB1157 (obtained from G. Walker) and MS23 (obtained from B. Sedgwick) to tetracycline resistance (Tetr) with a P1 vir lysate of strain NK5526 (obtained from B. Bachmann), which contains hisG2J3::TnlO.…”

Section: Methodsmentioning

confidence: 99%

Induction of transversion mutations in Escherichia coli by N-methyl-N'-nitro-N-nitrosoguanidine is SOS dependent

Foster¹,

Eisenstadt²

1985

J Bacteriol

View full text Add to dashboard Cite

Escherichia coli alkA mutants, which are deficient for an inducible DNA glycosylase, 3-methyladenine-DNA glycosylase II, are sensitive to mutagenesis by low doses of the alkylating agent N-methyl-N'-nitro-Nnitrosoguanidine (MNNG). As many as 90% of the alkA-dependent mutations induced by MNNG are also umuC+ dependent and thus are due to DNA lesions that are substrates for the mutagenic functions of the SOS response. A great number of these mutations are base substitutions at A T sites, particularly A. T transversions. We discuss which DNA lesions may be responsible for these mutations. Our results show that the induction of 3-methyladenine-DNA glycosylase II, which occurs as part of the adaptive response to alkylating agents such as MNNG, significantly reduces the mutagenicity as well as the lethality of alkylation damage. The biological consequences of exposing bacteria to DNA-alkylating agents depend on the chemical nature of the DNA damage induced. For example, alkylation of the 06 position of guanine creates a modified base with the coding properties of adenine (45). Thus, this lesion is highly and directly mutagenic, giving rise to G * C-to-A. T transitions (41). In contrast, alkylation of the N3 position of adenine creates a modified base that blocks the replication fork (8;

show abstract

Section: Methodsmentioning

confidence: 99%

Induction of transversion mutations in Escherichia coli by N-methyl-N'-nitro-N-nitrosoguanidine is SOS dependent

Foster¹,

Eisenstadt²

1985

J Bacteriol

View full text Add to dashboard Cite

show abstract

“…This enzyme has a broad in vitro substrate specificity and, in addition to 3-methyladenine, is able to release 3-methylguanine, 7-methylguanine, and 7-methyladenine from methylated DNA (155). 3-Methyladenine-DNA glycosylase II is the product of the alkA gene (96,162,375,376). E. coli has a second enzyme, 3-methyladenine-DNA glycosylase I, the product of the tag gene, which is only able to release 3methyladenine (96,157,191,280).…”

Section: Biochemistry Of the Adaptive Responsementioning

confidence: 99%

Mutagenesis and inducible responses to deoxyribonucleic acid damage in Escherichia coli.

Walker¹

1984

Microbiological Reviews

1,035

410

View full text Add to dashboard Cite

“…This operon is located at 47 min on the genetic map [Jeggo, 1979;Kataoka et al, 1983;Sedgwick 19821. The third gene is aZkA, which maps at 45 min [Yamamoto et al, 1978;Volkert et al, 19861. A fourth gene, uidB (95 min), is also part of the adaptive response, but its role in survival or mutagenesis has not been established [Volkert et al, 19861.…”

Section: Genetics Of the Adaptive Responsementioning

confidence: 99%

Adaptive response of escherichia coli to alkylation damage

Volkert

1988

Environ and Mol Mutagen

103

View full text Add to dashboard Cite

Treatment of cells with low levels of alkylating agents for extended periods of time causes them to become resistant to the lethal and mutagenic effects of subsequent high-level challenge treatments with alkylating agents. This increased resistance has been called the adaptive response to alkylation damage and results from the induction of an alkylation-specific DNA repair response. The adaptive response is most efficiently induced by methylating agents and is most effective against the lethal and mutagenic effects of methylation damage to DNA. Four genes have been identified as components of this response, ada, alkA, alkB and aidB. The functions of two of these genes are known. AlkA protein functions as a glycosylase that repairs N3-meA, N3-meG, O2-meT, and O2-meC residues in DNA, and Ada protein functions as an alkyltransferase that removes alkyl groups from O6-meG, O4-meT residues as well as methylphosphotriesters. After it interacts with methylated DNA, Ada protein functions as a positive regulatory element that controls the expression of the adaptive response by stimulating the expression of the ada-alkB operon, and the alkA and aidB genes.

show abstract

Escherichia coli gene that controls sensitivity to alkylating agents

Cited by 80 publications

References 12 publications

Induction of transversion mutations in Escherichia coli by N-methyl-N'-nitro-N-nitrosoguanidine is SOS dependent

Induction of transversion mutations in Escherichia coli by N-methyl-N'-nitro-N-nitrosoguanidine is SOS dependent

Mutagenesis and inducible responses to deoxyribonucleic acid damage in Escherichia coli.

Adaptive response of escherichia coli to alkylation damage

Contact Info

Product

Resources

About