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Evidence for a Rad18-independent frameshift mutagenesis pathway in human cell-free extracts.
PLoS One
September 2012
Université de Strasbourg, UMR7242 Biotechnologie et Signalisation Cellulaire, Ecole Supérieure de Biotechnologie de Strasbourg, Illkirch, France.
Bypass of replication blocks by specialized DNA polymerases is crucial for cell survival but may promote mutagenesis and genome instability. To gain insight into mutagenic sub-pathways that coexist in mammalian cells, we examined N-2-acetylaminofluorene (AAF)-induced frameshift mutagenesis by means of SV40-based shuttle vectors containing a single adduct. We found that in mammalian cells, as previously observed in E.
View Article and Find Full Text PDFMechanism of DNA polymerase II-mediated frameshift mutagenesis.
Proc Natl Acad Sci U S A
July 2001
UPR 9003 du Centre National de la Recherche Scientifique, Unité Propre de Recherche du CNRS conventionnée avec l'Université de Strasbourg, Institut de Recherche sur les Cancers de l'Appareil Digestif, Strasbourg, France.
Escherichia coli possesses three SOS-inducible DNA polymerases (Pol II, IV, and V) that were recently found to participate in translesion synthesis and mutagenesis. Involvement of these polymerases appears to depend on the nature of the lesion and its local sequence context, as illustrated by the bypass of a single N-2-acetylaminofluorene adduct within the NarI mutation hot spot. Indeed, error-free bypass requires Pol V (umuDC), whereas mutagenic (-2 frameshift) bypass depends on Pol II (polB).
View Article and Find Full Text PDFSequence determinants for -2 frameshift mutagenesis at NarI-derived hot spots.
J Mol Biol
October 1995
CNRS UPR #9003 Cancérogenèse et Mutagenèse Moléculaire et Structurale ESBS, Strasbourg-Illkirch, France.
The recognition sequence of the NarI restriction enzyme is known to be a strong hot spot for -2 frameshift mutations (G1G2CG3CC-->GGCC) induced by the chemical carcinogen N-2-acetylaminofluorene (AAF). In an attempt to define a "consensus sequence" for this mutation hot spot, we have investigated the role of the bases flanking the central dinucleotide GpC repeat in the NarI sequence (NaGCGCNb) on the mutation frequency induced by the carcinogen. Construction and random modification with AAF of the 16 plasmids resulting from the replacement of Na and Nb by A,T,G and C, respectively, have been undertaken.
View Article and Find Full Text PDFMutational spectrum induced in Saccharomyces cerevisiae by the carcinogen N-2-acetylaminofluorene.
Mol Gen Genet
October 1994
UPR Cancérogenèse et Mutagenèse Moléculaire et Structurale, IBMC CNRS, Strasbourg, France.
The spectrum of mutations induced by the carcinogen N-2-acetylaminofluorene (AAF) was analysed in Saccharomyces cerevisiae using a forward mutation assay, namely the inactivation of the URA3 gene. The URA3 gene, carried on a yeast/bacterial shuttle vector, was randomly modified in vitro using N-acetoxy-N-2-acetylaminofluorene (N-AcO-AAF) as a model reactive metabolite of the carcinogen AAF. The binding spectrum of AAF to the URA3 gene was determined and found to be essentially random, as all guanine residues reacted about equally well with N-AcO-AAF.
View Article and Find Full Text PDFStrong structural effect of the position of a single acetylaminofluorene adduct within a mutation hot spot.
Nucleic Acids Res
December 1989
Groupe de Cancérogénèse et de Mutagénèse Moléculaire et Structurale, IBMC du CNRS, Strasbourg, France.
The NarI restriction enzyme recognition site, G1G2CG3CC, has been identified as a hotspot for -2 frameshift mutations induced by N-2-acetylaminofluorene (AAF) on the basis of a forward mutation assay in plasmid pBR322 in the bacterium Escherichia coli. AAF binds primarily to the C-8 position of guanine residues, and the three guanines of the NarI site are similarly reactive. Despite this similar chemical reactivity, only binding of AAF to the G3 residue causes the -2 frameshift mutations.
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