MucAB but not UmuDC proteins enhance -2 frameshift mutagenesis induced by N-2-acetylaminofluorene at alternating GC sequences.
N-2-acetylaminofluorene has been shown efficiently to induce both -1 and -2 frameshift mutations in Escherichia coli as well as in mammalian cells. In E. coli, the genetic characteristics of -1 and -2 frameshift mutations were found to be distinct. The -1 frameshift mutation pathway occurs at monotonous runs of G residues (i.e. GGG-->GG). This pathway exhibits the same genetic requirements as UV light-induced base substitution mutagenesis. Indeed, optimal mutagenesis requires the expression of both UmuDC and the activated form of RecA. The -2 frameshift mutation pathway operates at short alternating GpC sequences, such as the NarI sequence (i.e. GGCGCC-->GGCC). In contrast to the -1 frameshift mutation pathway, optimal induction does not require the UmuDC and RecA proteins. This pathway involves a LexA-repressed function tentatively called Npf (for NarI processing factor). In this paper, we show that MucAB efficiently stimulates the -2 frameshift mutation pathway. However, unlike the Npf pathway, MucAB-mediated stimulation requires expression of the RecA protein.
Janel-Bintz
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R
Cancérogenèse et Mutagenèse Molèculaire et Structurale, UPR 9003 CNRS, Pôle API ESBS, Illkirch, France.
Maenhaut-Michel
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G
Fuchs
R P
RP
D015073:2-Acetylaminofluorene / Q000633:toxicity*; D001426:Bacterial Proteins / Q000502:physiology*; D003596:Cytosine; D004259:DNA-Directed DNA Polymerase; D004926:Escherichia coli / Q000187:drug effects* / Q000235:genetics / Q000502:physiology; D029968:Escherichia coli Proteins; D016368:Frameshift Mutation; D006147:Guanine; D011938:Rec A Recombinases / Q000378:metabolism
D001426:Bacterial Proteins; D029968:Escherichia coli Proteins; C068606:mucAB protein, E coli; D006147:Guanine; D003596:Cytosine; C078202:UmuC protein, E coli; D015073:2-Acetylaminofluorene; D011938:Rec A Recombinases; D004259:DNA-Directed DNA Polymerase; C055218:UmuD protein, E coli