Abstract:
:To study the mechanisms of mutagenesis by the carcinogen N-acetyl-2-aminofluorene (AAF), we determined by DNA sequencing the spectrum of mutations in the Escherichia coli lacI gene induced by the ultimate metabolite N-acetoxy-N-acetyl-2-aminofluorene, using an E. coli derivative with increased permeability to this compound. Several different classes of mutations were recovered, including base substitutions (11%), single-base frameshifts (11%), double-base frameshifts (22%), deletions (21%), duplications (2%) and 'spontaneous hot-spot' mutations [26%; the gain (19%) or loss (7%) of TGGC at the sequence TGGCTGGCTGGC]. Among the base substitutions, both transitions and transversions occurred. The single-base frameshifts were all the loss of a base. The double-base frameshifts represented the loss of a (GpC) or (ApC) dinucleotide from alternating (GpC)n or (ApC)n sequences. The deletion, duplication and hot-spot mutations showed relative G,C-richness at their endpoints, suggesting that AAF-induced lesions at or near the endpoints promoted their occurrence. Taken together, the data are consistent with several previous findings on AAF mutagenesis, extending in particular the importance of frameshift mutagenesis at alternating purine-pyrimidine sequences and establishing deletion and duplication mutations as an important consequence of treatment with this carcinogen.
journal_name
Carcinogenesisjournal_title
Carcinogenesisauthors
Schaaper RM,Koffel-Schwartz N,Fuchs RPdoi
10.1093/carcin/11.7.1087subject
Has Abstractpub_date
1990-07-01 00:00:00pages
1087-95issue
7eissn
0143-3334issn
1460-2180journal_volume
11pub_type
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