The mutagenic and lethal effects of monofunctional methylating agents in strains of Haemophilus influenzae defective in repair processes
| Autor: | Mini Liu, Jane K. Setlow, R.F. Kimball |
|---|---|
| Rok vydání: | 1971 |
| Předmět: |
DNA
Bacterial Alkylating Agents DNA Repair Guanine Cell Survival Ultraviolet Rays Health Toxicology and Mutagenesis Mutant Pyrimidine dimer Biology medicine.disease_cause Microbiology Haemophilus influenzae chemistry.chemical_compound Endonuclease Genetics medicine Radiation Genetics Molecular Biology Nitrosoguanidines Recombination Genetic Mutation Drug Resistance Microbial Nitro Compounds Molecular biology chemistry biology.protein Sulfonic Acids DNA Nucleotide excision repair Nitroso Compounds |
| Zdroj: | Mutation research. 12(1) |
| ISSN: | 0027-5107 |
| Popis: | 4 mutant strains of Haemophilus influenzae were tested for their response to the monofunctional methylating agents N-methyl-N′-nitrosoguanidine (MNNG) and methyls methanesulfonate (MMS). 2 of these strains are unable to excise pyrimidine dimers, 1 is slow in rejoining breaks produced by excision, and 1 is unable to support recombination or rejoin the single-strand breaks produced in DNA by X-rays. The 3 strains with defects in the excision repair process are like wild-type in their sensitivity to killing by the 2 agents; the recombinationless strain is more sensitive to both agents by a factor of 3–4. MMS does not induced a detectable number of mutations to cathomycin resistance at doses that give equal survival from mutagenic doses of MNNG and approximately equal numbers of induced single-strand breaks in the DNA. It is suggested that the mutation induced by MNNG is due to specific alteration—perhaps alkylation of guanine on the oxygen at the 6 position—produced by this agent but not by MMS. 3 of the strains, including the recombinationless one, give approximately the same mutation yield as wild-type with MNNG. 1 of the 2 excisionless strains gives a distinctly lower yield. This mutant has been shown earlier to lack the endonuclease that makes the initial incision for the excision repair process in DNA containing pyrimidine dimers. It is suggested that this endonuclease can also act on the MNNG-specific mutagenic alteration to enhance the probability that it will cause mutation. It seems improbable that the complete excision repair process is involved in this enhancement, or indeed that excision repair of biologically significant alterations produced by monofunctional alkylating agents occurs. |
| Databáze: | OpenAIRE |
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