Proficient deoxyribonucleic acid repair of methylation damage in hamster ERCC-gene mutants.
Mutat Res
; 407(3): 261-8, 1998 Jun.
Article
en En
| MEDLINE
| ID: mdl-9653452
Three major pathways, nucleotide excision repair (NER), base excision repair (BER) and O6-methylguanine-DNA methyltransferase (MGMT), are responsible for the removal of most adducts to DNA and thus for the survival of cells influenced by deoxyribonucleic acid (DNA) adduct-forming chemicals. We have evaluated host cell reactivation and cell survival of wild type Chinese hamster ovary cells and of mutants in the NER-genes ERCC1, ERCC2, and ERCC4 after treatment with the methylating compounds dimethylsulfate and methylnitrosourea. No effect of the three genes could be demonstrated, i.e., survival and host cell reactivation after methylation damage in the mutants and the wild type cells were similar. Gene-specific repair experiments confirmed the proficient removal of methyl lesions. We conclude that the three nucleotide excision repair genes are immaterial to the repair of methylation damage. This suggests that NER does not play a role in the removal of methylation in mammalian cells and that BER and MGMT are responsible for the survival of such cells, when they are challenged with methylation of DNA.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Proteínas
/
Proteínas de Unión al ADN
/
Reparación del ADN
/
Endonucleasas
/
Mutación
Límite:
Animals
Idioma:
En
Revista:
Mutat Res
Año:
1998
Tipo del documento:
Article
País de afiliación:
Dinamarca
Pais de publicación:
Países Bajos