Adaptive response of escherichia coli to alkylation damage

  title={Adaptive response of escherichia coli to alkylation damage},
  author={Michael R Volkert},
  journal={Environmental and Molecular Mutagenesis},
  • M. Volkert
  • Published 1988
  • Biology
  • Environmental and Molecular Mutagenesis
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… 

Inducible repair of alkylated DNA in microorganisms.

Mutagenesis and DNA repair for alkylation damages in Escherichia coli k‐12

It is proposed that the biological significance of the ogt protein relies mainly on its ability to prevent mutagenesis by low levels of bulkier ethylation products (especially in the absence of uvr excision repair).

Induction of the alkyltransferase (MGMT) gene by DNA damaging agents and the glucocorticoid dexamethasone and comparison with the response of base excision repair genes.

The induction of MGMT and other genes encoding enzymes involved in DNA alkylation damage repair may be relevant in cancer therapy by causing resistance of tumor cells to alkylating drugs.

Quasi-Adaptive Response to Alkylating Agents in Escherichia coli: A New Phenomenon

The new phenomenon extends the functional range of NO compounds to include a role in genetic signal transduction within the Ada response system in addition to similar roles in the SoxRS, SOS, and OxyR systems in E. coli.

The AidB Component of the Escherichia coli Adaptive Response to Alkylating Agents Is a Flavin-Containing, DNA-Binding Protein

On the basis of its ability to bind DNA and its possession of a redox-active flavin, AidB is predicted to catalyze the direct repair of alkylated DNA.



Induction of a DNA glycosylase for N-methylated purines is part of the adaptive response to alkylating agents

The resistance of Escherichia coli to simple alkylating agents, for example N-methyl-N′-nitro-N-nitrosoguanidine (MNNG), is markedly increased in cells previously exposed to low doses of the agents.

Adaptive response to alkylating agents involves alteration in situ of O6-methylguanine residues in DNA

It is reported that O6-MeG disappears from alkylated DNA after incubation with a crude enzyme fraction from adapted cells, although no concomitant release of the methyl group or theAlkylated base or nucleotide occurs, due to a previously unrecognised DNA repair mechanism involving enzyme-catalysed structural alteration of the alkylations.

Adaptation to alkylation resistance involves the induction of a DNA glycosylase

The data presented here show that killing adaptation can be ascribed to the induction of a DNA glycosylase, which releases the alkylation product 3-methyladenine from DNA in vitro as does the constitutive m3A DNA glyCosylase previously characterized by Riazuddin and Lindahl.

Induction of resistance to alkylating agents in E. coli: the ada+ gene product serves both as a regulatory protein and as an enzyme for repair of mutagenic damage.

Antibodies raised against homogeneous O6‐methylguanine‐DNA methyltransferase (the main repair activity for mutagenic damage in alkylated DNA) were found to cross‐react with this 37‐kd protein.

Pathways of mutagenesis and repair in Escherichia coli exposed to low levels of simple alkylating agents

It is shown here that error-prone repair is responsible for the majority of mutants formed after a large dose of alkylating agent, but it is unlikely that it contributes significantly to mutagenesis during exposure to low concentrations of these chemicals.

Repair and mutagenesis in Escherichia coli K-12 after exposure to various alkyl-nitrosoguanidines

The mutagenic and toxic effects of a series of N-alkyl-N'-nitro-N-nitrosoguanidines were examined in Escherichia coli K-12. The role of nucleotide excision repair, the SOS response, and the adaptive

Induction of specific Escherichia coli genes by sublethal treatments with alkylating agents.

  • M. VolkertD. C. Nguyen
  • Biology
    Proceedings of the National Academy of Sciences of the United States of America
  • 1984
Both aidA and aidB share with adaptive response a common regulatory mechanism involving the ada gene, and the growth phase-dependent control of the aidB fusions, however, is unaffected by ada, suggesting that a second regulatory mechanism exists that controls only aidB.

Multiple species of Bacillus subtilis DNA alkyltransferase involved in the adaptive response to simple alkylating agents

The proposition that ada mutants can be classified into two groups is supported and extended; one is defective only in the inducible synthesis of O6-methylguanine:DNA methyltransferase (22-kDa protein), and the other is deficient in the adaptive response in toto.

Regulatory mechanisms for induction of synthesis of repair enzymes in response to alkylating agents: ada protein acts as a transcriptional regulator.

A model for the molecular mechanism of adaptive response of Escherichia coli to alkylating agents is proposed, and a methylated form of Ada protein is prepared by an in vitro reaction and compared the activity with that of the normal, unmethylated form.