Genetics of mutagenesis in E. coli: Various combinations of translesion polymerases (Pol II, IV and V) deal with lesion/sequence context diversity

DNA Repair

Volumn 1, Issue 2, 2002, Pages 159-167

  Wagner, Jérôme ^a   Etienne, Hélène ^a   Janel Bintz, Régine ^b   Fuchs, Robert P P ^a,b  

^a UNIVERSITÉ DE STRASBOURG   (France)

^b ESBS   (France)

Author keywords

AAF; Frameshift hot spots; Lesion and sequence context effects; Oxidative lesions; Pol II; Pol IV; Pol V; Slippage mutagenesis

Indexed keywords

DNA DIRECTED DNA POLYMERASE ALPHA; ISOENZYME; METHYLENE BLUE; N (2 FLUORENYL)ACETAMIDE; BACTERIAL DNA; CARCINOGEN; DNA DIRECTED DNA POLYMERASE; DNA DIRECTED DNA POLYMERASE BETA; DNA POLYMERASE V, E COLI; ENZYME INHIBITOR; ESCHERICHIA COLI PROTEIN;

ARTICLE; CONTROLLED STUDY; DNA DAMAGE; DNA REPLICATION; DNA TEMPLATE; ESCHERICHIA COLI; FRAMESHIFT MUTATION; GENETIC VARIABILITY; MUTAGENESIS; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; DNA ADDUCT; DNA REPAIR; DRUG EFFECT; ENZYMOLOGY; GC RICH SEQUENCE; GENETICS; LIGHT; METABOLISM; OXIDATION REDUCTION REACTION; PHYSIOLOGY; RADIATION EXPOSURE;

2-ACETYLAMINOFLUORENE; CARCINOGENS; DNA ADDUCTS; DNA DAMAGE; DNA POLYMERASE BETA; DNA POLYMERASE II; DNA REPLICATION; DNA, BACTERIAL; DNA-DIRECTED DNA POLYMERASE; ENZYME INHIBITORS; ESCHERICHIA COLI; FRAMESHIFT MUTATION; GC RICH SEQUENCE; LIGHT; METHYLENE BLUE; MUTAGENESIS; OXIDATION-REDUCTION; SOS RESPONSE (GENETICS); SUPPORT, NON-U.S. GOV'T; ESCHERICHIA COLI PROTEINS;

ESCHERICHIA COLI;

EID: 0036012786     PISSN: 15687864     EISSN: None     Source Type: Journal    
DOI: 10.1016/S1568-7864(01)00012-X     Document Type: Article

References (19)

1. All three SOS-inducible DNA polymerases (Pol II, IV and V) are involved in induced mutagenesis
2. The many faces of DNA polymerases: Strategies for mutagenesis and for mutational avoidance
3. Replication of damaged DNA: Molecular defect in xeroderma pigmentosum variant cells
4. Hot spots of frameshift mutations induced by the ultimate carcinogen N-acetoxy-N-2-acetylaminofluorene
5. Carcinogen-induced mutation spectrum in wild-type, uvrA and umuC strains of Escherichia coli. Strain specificity and mutation-prone sequences
6. Induction of -2 frameshift mutations within alternating GC sequences by carcinogens that bind to the C8 position of guanine residues: Development of a specific mutation assay
7. Frameshift mutagenesis induced in Escherichia coli after in vitro treatment of double-stranded DNA with methylene blue plus white light: Evidence for the involvement of lesion(s) other than 8-oxo-7,8-dihydro-2′-deoxyguanosine
8. 8-(N-2-fluorenylacetamido)guanosine, an arylamidation reaction product of guanosine and the carcinogen N-acetoxy-N-2-fluorenylacetamide in neutral solution
9. A umuDC-independent SOS pathway for frameshift mutagenesis
10. DNA polymerases II and V mediate, respectively, mutagenic (-2 frameshift) and error-free bypass of a single N-2-acetylaminofluorene adduct
11. Single adduct mutagenesis: Strong effect of the position of a single acetylaminofluorene adduct within a mutation hot spot
12. SOS factors involved in translesion synthesis
13. Mechanism of DNA polymerase II-mediated frameshift mutagenesis
14. Crystal structure of a Y-family DNA polymerase in action. A mechanism for error-prone and lesion-bypass replication
15. Involvement of E. coli DNA polymerase II in response to oxidative damage and adaptive mutation
16. Multiple pathways for SOS-induced mutagenesis in Escherichia coli: An overexpression of dinB/dinP results in strongly enhancing mutagenesis in the absence of any exogenous treatment to damage DNA
17. Construction of a umuDC operon substitution mutation in E. coli
18. Construction of frameshift mutation hot spots within the tetracycline resistance gene of pBR322
19. Cellular strategies for accommodating replication-hindering adducts in DNA: Control by the SOS response in Escherichia coli