Polymorphism in N-2-acetylaminofluorene induced DNA structure as revealed by DNase I footprinting.
Identifieur interne : 000689 ( Ncbi/Merge ); précédent : 000688; suivant : 000690Polymorphism in N-2-acetylaminofluorene induced DNA structure as revealed by DNase I footprinting.
Auteurs : X. Veaute [France] ; R P FuchsSource :
- Nucleic acids research [ 0305-1048 ] ; 1991.
Descripteurs français
- KwdFr :
- MESH :
English descriptors
- KwdEn :
- MESH :
- chemical , chemistry : 2-Acetylaminofluorene, DNA.
- chemical , metabolism : Deoxyribonuclease I.
- Base Sequence, DNA Damage, Molecular Sequence Data, Mutation, Nucleic Acid Conformation, Polymorphism, Genetic.
Abstract
In this paper, we have constructed double stranded helices (60-mers) containing a single N-2-acetylaminofluorene (-AAF) adduct covalently bound to one of the three guanine residues of the Narl site (G1G2CG3CC). This sequence was identified as a strong frameshift mutation hot spot for many carcinogens that bind to the C8 position of guanine. Using DNase I as a probe for DNA conformation we show i) that the average size of the helix deformation extends over 3 to 5 base pairs in both directions from the adduct site, and ii) that there is a strong polymorphism in the adduct induced DNA conformation. The present study supports the idea that adducts induce specific sequence dependent local conformational changes in DNA that are differentially recognized and processed by the enzymatic machineries that lead to repair or mutagenesis.
DOI: 10.1093/nar/19.20.5603
PubMed: 1945836
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pubmed:1945836Le document en format XML
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<term>Deoxyribonuclease I (metabolism)</term>
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<term>Deoxyribonuclease I (métabolisme)</term>
<term>Données de séquences moléculaires</term>
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<front><div type="abstract" xml:lang="en">In this paper, we have constructed double stranded helices (60-mers) containing a single N-2-acetylaminofluorene (-AAF) adduct covalently bound to one of the three guanine residues of the Narl site (G1G2CG3CC). This sequence was identified as a strong frameshift mutation hot spot for many carcinogens that bind to the C8 position of guanine. Using DNase I as a probe for DNA conformation we show i) that the average size of the helix deformation extends over 3 to 5 base pairs in both directions from the adduct site, and ii) that there is a strong polymorphism in the adduct induced DNA conformation. The present study supports the idea that adducts induce specific sequence dependent local conformational changes in DNA that are differentially recognized and processed by the enzymatic machineries that lead to repair or mutagenesis.</div>
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<Abstract><AbstractText>In this paper, we have constructed double stranded helices (60-mers) containing a single N-2-acetylaminofluorene (-AAF) adduct covalently bound to one of the three guanine residues of the Narl site (G1G2CG3CC). This sequence was identified as a strong frameshift mutation hot spot for many carcinogens that bind to the C8 position of guanine. Using DNase I as a probe for DNA conformation we show i) that the average size of the helix deformation extends over 3 to 5 base pairs in both directions from the adduct site, and ii) that there is a strong polymorphism in the adduct induced DNA conformation. The present study supports the idea that adducts induce specific sequence dependent local conformational changes in DNA that are differentially recognized and processed by the enzymatic machineries that lead to repair or mutagenesis.</AbstractText>
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