A new ATP-independent DNA endonuclease from<i>Schizosaccharomyces pombe</i>that recognizes cyclobutane pyrimidine dimers and 6–4 photoproducts

Bowman, Krista K.; Sidik, Khalifah; Smith, Colin A.; Taylor, John‐Stephen; Doetsch, Paul W.; Freyer, Greg A.

doi:10.1093/nar/22.15.3026

Cited by 90 publications

(76 citation statements)

References 23 publications

(15 reference statements)

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“…In several strains of S. pombe deleted in one of the NER genes, cyclobutane pyrimidine dimers (CPD) and 6-4 pyrimidine pyrimidone photoproducts (6-4 photoproducts) were efficiently removed from UV-damaged DNA (McCready et al 1993). In addition, an enzymatic activity introducing a nick immediately 5 0 to CPD and 6-4 photoproducts was reported in S. pombe cell extracts (Bowman et al 1994). In the filamentous fungus Neurospora crassa, a mutant mus18 strain was isolated that was specifically sensitive to UV, suggesting the presence of a novel repair process for UV lesions in N. crassa.…”

Section: Nicking Activity and Genes Encoding Uvdementioning

confidence: 99%

Alternative Excision Repair Pathways

Yasui

2013

Cold Spring Harbor Perspectives in Biology

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Alternative excision repair (AER) is a category of excision repair initiated by a single nick, made by an endonuclease, near the site of DNA damage, and followed by excision of the damaged DNA, repair synthesis, and ligation. The ultraviolet (UV) damage endonuclease in fungi and bacteria introduces a nick immediately 5 0 to various types of UV damage and initiates its excision repair that is independent of nucleotide excision repair (NER). Endo IVtype apurinic/apyrimidinic (AP) endonucleases from Escherichia coli and yeast and human Exo III-type AP endonuclease APEX1 introduce a nick directly and immediately 5 0 to various types of oxidative base damage besides the AP site, initiating excision repair. Another endonuclease, endonuclease V from bacteria to humans, binds deaminated bases and cleaves the phosphodiester bond located 1 nucleotide 3 0 of the base, leading to excision repair. A singlestrand break in DNA is one of the most frequent types of DNA damage within cells and is repaired efficiently. AER makes use of such repair capability of single-strand breaks, removes DNA damage, and has an important role in complementing BER and NER.N ER and base excision repair (BER) are the major excision repair pathways present in almost all organisms. In NER, dual incisions are introduced, the damaged DNA between the incised sites is then removed, and DNA synthesis fills the single-stranded gap, followed by ligation. In BER, an AP site, formed by depurination or created by a base damage-specific DNA glycosylase, is recognized by an AP endonuclease that introduces a nick immediately 5 0 to the AP site, followed by repair synthesis, removal of the AP site, and final ligation. Besides these two fundamental excision repair systems, investigators have found another category of excision repair-AER-an example of which is the excision repair of UV damage, initiated by an endonuclease called UV damage endonuclease (UVDE).UVDE introduces a single nick immediately 5 0 to various types of UV lesions as well as other types of base damage, and this nick leads to the removal of the lesions by an AER process designated as UVDE-mediated excision repair (UVER or UVDR). Genetic analysis in Schizosaccharomyces pombe indicates that UVER provides cells with an extremely rapid removal of UV lesions, which is important for cells exposed to UV in their growing phase.Endo IV-type AP endonucleases from Escherichia coli and budding yeast and the Exo III -type human AP endonuclease APEX1 are able to introduce a nick at various types of oxidative base damage and initiate a form of excision repair that has been designated as nucleotide incision repair (NIR). Endonuclease V

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Section: Nicking Activity and Genes Encoding Uvdementioning

confidence: 99%

Alternative Excision Repair Pathways

Yasui

2013

Cold Spring Harbor Perspectives in Biology

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“…For the two extra ring pBQ-adducts, the AP endonucleases may serve as damage-specific endonucleases, initiating a process similar to the so-called alternative excision repair pathway. (108,109) This mechanism seems to be limited as AP endonucleases have not been found to act on five-and six-membered adducts. Overlapping repair also exists for some exocyclic adducts, since, chemically, most of the exocyclic adducts are nonbulky, which makes them potential targets for various pathways.…”

Section: Discussionmentioning

confidence: 99%

“…A similar mechanism, namely, alternative excision repair, was previously proposed for a damage-specific endonuclease-initiated repair of thymine dimer and other lesions in S. pombe. (108,109) Recently, both bacterial and human AP endonucleases were found to act on several oxidized bases (Fig. 4) using a similar mode of action.…”

Section: Repair Of Six-membered Propano-g Derivatives and M 1 G By Thmentioning

confidence: 90%

Repair of exocyclic DNA adducts: rings of complexity

Hang

2004

BioEssays

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SummaryExocyclic DNA adducts are mutagenic lesions that can be formed by both exogenous and endogenous mutagens/ carcinogens. These adducts are structurally analogs but can differ in certain features such as ring size, conjugation, planarity and substitution. Although the information on the biological role of the repair activities for these adducts is largely unknown, considerable progress has been made on their reaction mechanisms, substrate specificities and kinetic properties that are affected by adduct structures. At least four different mechanisms appear to have evolved for the removal of specific exocyclic adducts. These include base excision repair, nucleotide excision repair, mismatch repair, and AP endonuclease-mediated repair. This overview highlights the recent progress in such areas with emphasis on structure-activity relationships. It is also apparent that more information is needed for a better understanding of the biological and structural implications of exocyclic adducts and their repair.

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“…One is the T4denV type that is a pyrimidine dimer glycosylase/AP lyase resembling the base excision mechanism for alkylation and oxidative damage [6]. The other is a UV endonuclease that cleaves the phosphodiester bond 5 to a dimer [7,8].…”

Section: Do We Know All Possible Strategies For Ner In All Organisms?mentioning

confidence: 99%

Nucleotide excision repair “a legacy of creativity”

Cleaver

Karplus

Kashani‐Sabet

et al. 2001

Mutation Research/DNA Repair

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The first half of the 20th century has seen an enormous growth in our knowledge of DNA repair, in no small part due to the work of Dirk Bootsma, Philip Hanawalt and Bryn Bridges; those honored by this issue. For the new millennium, we have asked three general questions: (A) Do we know all possible strategies of nucleotide excision repair (NER) in all organisms? (B) How is NER integrated and regulated in cells and tissues? (C) Does DNA replication represent a new frontier in the roles of DNA repair? We make some suggestions for the kinds of answers the next generation may provide. The kingdom of archea represents an untapped field for investigation of DNA repair in organisms with extreme lifestyles. NER appears to involve a similar strategy to the other kingdoms of prokaryotes and eukaryotes, but subtle differences suggest that individual components of the system may differ. NER appears to be regulated by several major factors, especially p53 and Rb which interact with transcription coupled repair and global genomic repair, respectively. Examples can be found of major regulatory changes in repair in testicular tissue and melanoma cells. Our understanding of replication of damaged DNA has undergone a revolution in recent years, with the discovery of multiple low-fidelity DNA polymerases that facilitate replicative bypass. A secondary mechanism of replication in the absence of NER or of one or more of these polymerases involves sister chromatid exchange and recombination (hMre11/hRad50/Nbs1). The relative importance of bypass and recombination is determined by the action of p53. We hypothesise that these polymerases may be involved in resolution of complex DNA structures during completion of replication and sister chromatid resolution. With these fascinating problems to investigate, the field of DNA repair will surely not disappoint the next generation.

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A new ATP-independent DNA endonuclease fromSchizosaccharomyces pombethat recognizes cyclobutane pyrimidine dimers and 6–4 photoproducts

Cited by 90 publications

References 23 publications

Alternative Excision Repair Pathways

Alternative Excision Repair Pathways

Repair of exocyclic DNA adducts: rings of complexity

Nucleotide excision repair “a legacy of creativity”

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