You are not currently logged in.
Access your personal account or get JSTOR access through your library or other institution:
If You Use a Screen ReaderThis content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Single Adduct Mutagenesis: Strong Effect of the Position of a Single Acetylaminofluorene Adduct within a Mutation Hot Spot
Dominique Burnouf, Patrice Koehl and Robert P. P. Fuchs
Proceedings of the National Academy of Sciences of the United States of America
Vol. 86, No. 11 (Jun. 1, 1989), pp. 4147-4151
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/33641
Page Count: 5
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Preview not available
2-Acetylaminofluorene (AAF), a potent rat liver carcinogen that binds covalently to the C-8 position of guanine residues in DNA, is an effective frameshift mutagen. The mutations are distributed nonrandomly, in that most are located at a few specific DNA sequence (i.e., mutation hot spots). Among these hot spots, the Nar I sequence (GGCGCC) is especially susceptible to the induction of -2 frameshift mutations (GGCGCC → GGCC). Due to the nature of the Nar I sequence, G1G2CG3CC, three different molecular events, each involving the deletion of two contiguous base pairs (i.e., G2C, CG3, G3C), can give rise to the observed end point (GGCC). To compare the potential role of each of the three possible guanine-AAF adducts in the Nar I site to induce the -2 frameshift mutation, we constructed double-stranded plasmid molecules containing a single-AAF adduct bound to one of the three guanine positions. Using these plasmids, we found that only the adduct in the G3 position induces the -2 frameshift mutation. This strong effect of the position of the -AAF adduct within the Nar I site is discussed in relation to the possible involvement of an unusual DNA conformation in the mutagenic processing.
Proceedings of the National Academy of Sciences of the United States of America © 1989 National Academy of Sciences