2004
DOI: 10.1016/j.dnarep.2003.11.012
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A role for DNA polymerase V in G→T mutations from the major benzo[a]pyrene N2-dG adduct when studied in a 5′-TT sequence in E. coli

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Cited by 29 publications
(34 citation statements)
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“…However, induction of the SOS response in E. coli increases bypass of bulky adducts, including (ϩ)-ta[BP]G, with a significant increase in both error-free and error-prone events (49,51,60,66); this suggests that Y-family DNA polymerases, including pol IV and pol V, evolved to overcome replication hurdles in order to increase cellular survival (6,60). In agreement, a recent study suggests two mutagenic pathways for G 3 T mutations in E. coli dictated by sequence context, one of which is dependent on DNA polymerase V, a Y-family DNA polymerase (67). Indeed, bulky adducts, such as (ϩ)-ta[BP]G, predominantly block replicative DNA polymerases (47, 56 -58, 68 -70), but members of the Y-family, including pol (71), pol (64), and pol (63), bypass these adducts more readily than their replicative counterparts, albeit with reduced efficiency when compared with that in undamaged DNA (4,7,20,63,71).…”
supporting
confidence: 68%
“…However, induction of the SOS response in E. coli increases bypass of bulky adducts, including (ϩ)-ta[BP]G, with a significant increase in both error-free and error-prone events (49,51,60,66); this suggests that Y-family DNA polymerases, including pol IV and pol V, evolved to overcome replication hurdles in order to increase cellular survival (6,60). In agreement, a recent study suggests two mutagenic pathways for G 3 T mutations in E. coli dictated by sequence context, one of which is dependent on DNA polymerase V, a Y-family DNA polymerase (67). Indeed, bulky adducts, such as (ϩ)-ta[BP]G, predominantly block replicative DNA polymerases (47, 56 -58, 68 -70), but members of the Y-family, including pol (71), pol (64), and pol (63), bypass these adducts more readily than their replicative counterparts, albeit with reduced efficiency when compared with that in undamaged DNA (4,7,20,63,71).…”
supporting
confidence: 68%
“…1C). This mechanism clearly supports a link between base substitutions and frameshift mutations and suggests a straightforward explanation for 5Ј sequence dependence in base substitutions induced by the bulky adducts in E. coli (2,12,30,32).…”
Section: Bp-dg Looping-out and ؊1 Frameshift Mutationsmentioning
confidence: 79%
“…In consequence, the base 5Ј determines the identity of the base incorporated opposite the lesion, which is referred as the 5Ј rule (20). The mutations induced by BP-dG in Escherichia coli are Ͼ95% G 3 T in a 5Ј-TG*C sequence and Ͼ95% G 3 A in a 5Ј-AG*A sequence, respectively, which follow the 5Ј rule and are Y-family polymerase-dependent (12,29,30). The 5Ј rule is also clearly demonstrated by the present replication assays on templates that have four different bases 5Ј to the BP-dG lesion (Fig.…”
Section: Bp-dg Looping-out and ؊1 Frameshift Mutationsmentioning
confidence: 99%
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“…These lesions can produce mutations on replication in vitro and in vivo [74][75][76]. Such mutations, when present in DNA sequences that regulate the cell cycle, can trigger cancer initiation [72].…”
Section: Box 3 Benzo[a]pyrene-derived Dna Lesionsmentioning
confidence: 99%