DNA polymerases II and V mediate respectively mutagenic (-2 frameshift) and error-free bypass of a single N-2-acetylaminofluorene adduct

Fuchs, R. P. P., Koffel-Schwartz, N., Pelet, S., Janel-Bintz, R., Napolitano, R., Becherel, O. J., Broschard, T. H., Burnouf, D. Y. and Wagner, J. (2001) DNA polymerases II and V mediate respectively mutagenic (-2 frameshift) and error-free bypass of a single N-2-acetylaminofluorene adduct. Biochemical Society. Transactions, 29 2: 191-195. doi:10.1042/bst0290191


Author Fuchs, R. P. P.
Koffel-Schwartz, N.
Pelet, S.
Janel-Bintz, R.
Napolitano, R.
Becherel, O. J.
Broschard, T. H.
Burnouf, D. Y.
Wagner, J.
Title DNA polymerases II and V mediate respectively mutagenic (-2 frameshift) and error-free bypass of a single N-2-acetylaminofluorene adduct
Journal name Biochemical Society. Transactions   Check publisher's open access policy
ISSN 0300-5127
1470-8752
Publication date 2001-05-01
Year available 2001
Sub-type Article (original research)
DOI 10.1042/bst0290191
Open Access Status Not Open Access
Volume 29
Issue 2
Start page 191
End page 195
Total pages 5
Place of publication London, United Kingdom
Publisher Portland Press
Language eng
Formatted abstract
The Nar1 sequence represents a strong mutation hot spot for - 2 frameshift mutations induced by N-2-acetylaminofluorene (AAF), a strong chemical carcinogen. Only when bound to the third (underlined) guanine (5'-GGCGCC → GGCC) can AAF trigger frameshift mutations, suggesting the involvement of a slipped replication intermediate with a two-nucleotide bulge. While base substitutions induced by UV light or abasic sites require DNA polymerase V (Pol V; umuDC), the AAF-induced - 2 frameshift pathway requires DNA polymerase II, the polB gene product. Interestingly, error-free bypass of the G-AAF adduct requires Pol V. The genes encoding both Pol II and Pol V are induced by the SOS regulon, a co-ordinated cellular response to environmental stress. A given lesion, G-AAF, can thus be bypassed by two SOS-controlled DNA polymerases (II and V), generating mutagenic ( - 2 frameshifts) and error-free replication products respectively. Therefore both Pol II and Pol V can compete for the blocked replication intermediate in the vicinity of the lesion and engage in replication by transiently replacing the replicative DNA Pol III. Our data suggest that, in order to cope with the large diversity of existing DNA lesions, cells use a single or a combination of translesional DNA polymerases to achieve translesion synthesis.
Keyword DNA polymerase switches
PolB
Slippage mutagenesis
Translesional DNA polymerases
UmuDC
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Chemistry and Molecular Biosciences
 
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Created: Tue, 09 Aug 2016, 16:12:51 EST by Olivier Becherel on behalf of School of Chemistry & Molecular Biosciences