Enzymatic Repair of DNA

Grossman, L.; Braun, Andrew G.; Feldberg, Ross S.; Mahler, Inga

doi:10.1146/annurev.bi.44.070175.000315

Cited by 203 publications

(66 citation statements)

References 60 publications

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“…In all three cases, the overall pattern of repair synthesis is suggestive of a repair system which is integrally associated with DNA replication, or is dependent on enzymes induced in a co-ordinate fashion. Indeed, there is evidence that induction of enzymes occurs as DNA replication increases (25)(26)(27); a number of these enzymes has been implicated in DNA repair (28).…”

Section: Resultsmentioning

confidence: 99%

Repair of ionizing radiation induced DNA damage In human lymphocytes

Lavin

Kidson

1977

Nucl Acids Res

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Section: Resultsmentioning

confidence: 99%

Repair of ionizing radiation induced DNA damage In human lymphocytes

Lavin

Kidson

1977

Nucl Acids Res

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“…Earlier studies showed that, although the majority of UV lesions in Escherichia coli result in short repair patches of ∼20-30 nt, a small proportion leads to long patches of up to several hundred nucleotides (42). In addition, mutants deficient in polymerase I or its 5′ exonuclease activity led to more long patches that were proposed to be due to gap expansion by a 3′ exonuclease and resynthesis by DNA polymerases II or III (42,43). The polymerases II and III had been shown to generate longer patches than polymerase I (44).…”

Section: Compromised Tls Activity Leads To Increased Recombinant Molementioning

confidence: 99%

Homologous recombination rescues ssDNA gaps generated by nucleotide excision repair and reduced translesion DNA synthesis in yeast G2 cells

Westmoreland

Resnick

2013

Proc. Natl. Acad. Sci. U.S.A.

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Repair of DNA bulky lesions often involves multiple repair pathways such as nucleotide-excision repair, translesion DNA synthesis (TLS), and homologous recombination (HR). Although there is considerable information about individual pathways, little is known about the complex interactions or extent to which damage in single strands, such as the damage generated by UV, can result in double-strand breaks (DSBs) and/or generate HR. We investigated the consequences of UV-induced lesions in nonreplicating G2 cells of budding yeast. In contrast to WT cells, there was a dramatic increase in ssDNA gaps for cells deficient in the TLS polymerases η (Rad30) and ζ (Rev3). Surprisingly, repair in TLS-deficient G2 cells required HR repair genes RAD51 and RAD52, directly revealing a redundancy of TLS and HR functions in repair of ssDNAs. Using a physical assay that detects recombination between circular sister chromatids within a few hours after UV, we show an approximate three-fold increase in recombinants in the TLS mutants over that in WT cells. The recombination, which required RAD51 and RAD52, does not appear to be caused by DSBs, because a dose of ionizing radiation producing 20 times more DSBs was much less efficient than UV in producing recombinants. Thus, in addition to revealing TLS and HR functional redundancy, we establish that UV-induced recombination in TLS mutants is not attributable to DSBs. These findings suggest that ssDNA that might originate during the repair of closely opposed lesions or of ssDNA-containing lesions or from uncoupled replication may drive recombination directly in various species, including humans.

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“…It has been generally assumed that repair of pyrimidine dimers introduced into DNA by UV irradiation occurs by a nucleotide excision mechanism initiated by a specific endonuclease (1). Such endonucleases are known as UV endonucleases, and have been found in various organisms, including Escherichia coli (2,3), Micrococcus luteus (4), and bacteriophage T4 (5).…”

mentioning

confidence: 99%

Apurinic/apyrimidinic endonucleases in repair of pyrimidine dimers and other lesions in DNA.

Warner¹,

Demple²,

Deutsch³

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

152

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The characteristics of the nicks (single-strand breaks) introduced into damaged DNA by Escherichia coli endonucleases III, IV, and VI and by phage T4 UV endonuclease have been investigated with E coli DNA polymerase I (DNA nucleotidyltransferase) Nicks introduced into depurinated DNA by endonuclease IV or VI provide good primer termini for the polymerase, whereas nicks introduced into depurinated DNA by endonuclease III or into irradiated DNA by T4 UV endonuclease do not. This result suggests that endonuclease IV nigks depurinated DNA on the 5' side of the apurinic site, as dOes endonuclease VI, whereas endonuclease III has a different incision mechanism. T4 UV endonuclease also possesses apurinic endonuclease activity that generates nicks in depurinated DNA with low priming activity for the polymerase. The priming activity of DNA nicked with endonuclease III or T4 UV endonuclease can be enhanced by an additional incubation with endonuclease VI and, to a lesser extent, by incubation with endonuclease IV. These results indicate that endonuclease III and T4 UV endonuclease (acting upon depurinated and irradiated DNA, respectively) generate nicks containing apurinic/ apyrimidinic sites at their 3' termini and that such sites are not rapidly excised by the 3' -5' activity of DNA polymerase I. However, endonuclease IV or VI apparently can remove such terminal apurinic/apyrimidinic sites as well as cleave on the 5' side of the unnicked sites. These results suggest roles for endonucleases III, IV, and VI in the repair of apurinic/apyrimidinic sites as well as pyrimidine dimer sites in DNA. Our results with T4 UV endonuclease suggest that the incision of irradiated DNA by T4 UV endonuclease involves both cleavage of the glycosylic bond at the 5' half of the pyrimidine dimer and cleavage of the phosphodiester bond originally linking the two nucleotides of the dimer. They also imply that the glycosylic bond is cleaved before the phosphodiester bond.It has been generally assumed that repair of pyrimidine dimers introduced into DNA by UV irradiation occurs by a nucleotide excision mechanism initiated by a specific endonuclease (1). Such endonucleases are known as UV endonucleases, and have been found in various organisms, including Escherichia coli (2, 3), Micrococcus luteus (4), and bacteriophage T4 (5). The specific incision generates a nick (single-strand break) consisting of a 3'-hydroxyl terminus and a 5'-phosphoryl terminus (6, 7), but the exact nature and location of this nick have not been elucidated. If it is located near the 5' side of the dimer, the dimer could then be removed by an exonuclease activity such as E. coil exonuclease VII (8) or the 5' --3' exonuclease of DNA polymerase I (DNA nucleotidyltransferase) (9), and repair could be completed by DNA polymerase and DNA ligase activities.The repair of DNA containing apyrimidinic or apurinic (AP) sites is also initiated by incision of the DNA by a specific endonuclease (10). Such AP sites may be generated either by DNA glycosylases (11) or by spontaneo...

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Enzymatic Repair of DNA

Cited by 203 publications

References 60 publications

Repair of ionizing radiation induced DNA damage In human lymphocytes

Repair of ionizing radiation induced DNA damage In human lymphocytes

Homologous recombination rescues ssDNA gaps generated by nucleotide excision repair and reduced translesion DNA synthesis in yeast G2 cells

Apurinic/apyrimidinic endonucleases in repair of pyrimidine dimers and other lesions in DNA.

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