The hypermutability conferred by the mus308 mutation of Drosophila is not specific for cross-linking agents

The hypersensitivity of the mus308 mutant of D. melanogaster to cross-linking agents has been suggested to be the consequence of a possible defect of this mutant in DNA cross-link repair. Moreover, the mus308 mutation has been proposed as an animal model for the study of Fanconi's anemia. In or...

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Bibliographic Details
Published in:Mutation research. DNA repair 1995-05, Vol.336 (3), p.243-250
Main Authors: Aguirrezabalaga, Ignacio, María Sierra, L., Comendador, Miguel A.
Format: Article
Language:English
Subjects:
Biological and medical sciences
DNA cross-links
Drosophila melanogaster
Fundamental and applied biological sciences. Psychology
Hypermutability
Molecular and cellular biology
Molecular genetics
mus308
Mutagenesis. Repair
Post-replication repair
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Summary:The hypersensitivity of the mus308 mutant of D. melanogaster to cross-linking agents has been suggested to be the consequence of a possible defect of this mutant in DNA cross-link repair. Moreover, the mus308 mutation has been proposed as an animal model for the study of Fanconi's anemia. In order to obtain more information about the function controlled by this locus, we have measured the mutability of the mus308 mutant to several mutagens with different modes of action using the sex-linked recessive lethal test. We show that this mutation confers hypermutability not only to the cross-linking agents tested, hexamethylphosphoramide and hexamethylmelamine, but to the point mutagen N-ethyl-N-nitrosourea as well, whereas the response to methyl methanesulfonate was normal. The results suggest that the mus308 locus is not defective in a repair pathway specific for cross-links but is rather involved in a step of a more general post-replication repair process responsible for the removal of non-excised adducts.
ISSN:0921-8777
1386-1476
DOI:10.1016/0921-8777(94)00057-D