scholarly journals The Roles of Several Residues ofEscherichia coliDNA Photolyase in the Highly Efficient Photo-Repair of Cyclobutane Pyrimidine Dimers

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Lei Xu ◽  
Guoping Zhu
Keyword(s):  
Escherichia Coli ◽  
Energy Source ◽  
Pyrimidine Dimer ◽  
Cyclobutane Pyrimidine Dimer ◽  
Model Compounds ◽  
Cyclobutane Pyrimidine Dimers ◽  
Dna Photolyase ◽  
Pyrimidine Dimers ◽  
Repair Efficiency ◽  
Very High

Escherichia coliDNA photolyase is an enzyme that repairs the major kind of UV-induced lesions, cyclobutane pyrimidine dimer (CPD) in DNA utilizing 350–450 nm light as energy source. The enzyme has very high photo-repair efficiency (the quantum yield of the reaction is ~0.85), which is significantly greater than many model compounds that mimic photolyase. This suggests that some residues of the protein play important roles in the photo-repair of CPD. In this paper, we have focused on several residues discussed their roles in catalysis by reviewing the existing literature and some hypotheses.

scholarly journals The effect of flanking bases on direct and triplet sensitized cyclobutane pyrimidine dimer formation in DNA depends on the dipyrimidine, wavelength and the photosensitizer

2021 ◽  
Author(s):  
Chen Lu ◽  
Natalia Eugenia Gutierrez-Bayona ◽  
John-Stephen Taylor
Keyword(s):  
Uv Light ◽  
Pyrimidine Dimer ◽  
Flanking Sequence ◽  
Quenching Mechanism ◽  
Cyclobutane Pyrimidine Dimers ◽  
Sequence Dependence ◽  
Pyrimidine Dimers ◽  
Skin Cancers ◽  
A Charge ◽  
C To T Mutations

Abstract Cyclobutane pyrimidine dimers (CPDs) are the major products of DNA produced by direct absorption of UV light, and result in C to T mutations linked to human skin cancers. Most recently a new pathway to CPDs in melanocytes has been discovered that has been proposed to arise from a chemisensitized pathway involving a triplet sensitizer that increases mutagenesis by increasing the percentage of C-containing CPDs. To investigate how triplet sensitization may differ from direct UV irradiation, CPD formation was quantified in a 129-mer DNA designed to contain all 64 possible NYYN sequences. CPD formation with UVB light varied about 2-fold between dipyrimidines and 12-fold with flanking sequence and was most frequent at YYYR and least frequent for GYYN sites in accord with a charge transfer quenching mechanism. In contrast, photosensitized CPD formation greatly favored TT over C-containing sites, more so for norfloxacin (NFX) than acetone, in accord with their differing triplet energies. While the sequence dependence for photosensitized TT CPD formation was similar to UVB light, there were significant differences, especially between NFX and acetone that could be largely explained by the ability of NFX to intercalate into DNA.

scholarly journals Photolyases from Saccharomyces cerevisiae and Escherichia coli recognize common binding determinants in DNA containing pyrimidine dimers.

1989 ◽  
Vol 9 (11) ◽  
pp. 4777-4788 ◽  
Author(s):  
M Baer ◽  
G B Sancar
Keyword(s):  
Escherichia Coli ◽  
Saccharomyces Cerevisiae ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Spectroscopic Studies ◽  
Pyrimidine Dimer ◽  
Nucleotide Sequence Analysis ◽  
Binding Motif ◽  
Pyrimidine Dimers ◽  
Nucleotide Excision

DNA photolyases catalyze the light-dependent repair of pyrimidine dimers in DNA. The results of nucleotide sequence analysis and spectroscopic studies demonstrated that photolyases from Saccharomyces cerevisiae and Escherichia coli share 37% amino acid sequence homology and contain identical chromophores. Do the similarities between these two enzymes extend to their interactions with DNA containing pyrimidine dimers, or does the organization of DNA into nucleosomes in S. cerevisiae necessitate alternative or additional recognition determinants? To answer this question, we used chemical and enzymatic techniques to identify the contacts made on DNA by S. cerevisiae photolyase when it is bound to a pyrimidine dimer and compared these contacts with those made by E. coli photolyase and by a truncated derivative of the yeast enzyme when bound to the same substrate. We found evidence for a common set of interactions between the photolyases and specific phosphates in the backbones of both strands as well as for interactions with bases in both the major and minor grooves of dimer-containing DNA. Superimposed on this common pattern were significant differences in the contributions of specific contacts to the overall binding energy, in the interactions of the enzymes with groups on the complementary strand, and in the extent to which other DNA-binding proteins were excluded from the region around the dimer. These results provide strong evidence both for a conserved dimer-binding motif and for the evolution of new interactions that permit photolyases to also act as accessory proteins in nucleotide excision repair. The locations of the specific contacts made by the yeast enzyme indicate that the mechanism of nucleotide excision repair in this organism involves incision(s) at a distance from the pyrimidine dimer.

phrA, the major photoreactivating factor in the cyanobacterium Synechocystis sp. strain PCC 6803 codes for a cyclobutane-pyrimidine-dimer-specific DNA photolyase

2000 ◽  
Vol 173 (5-6) ◽  
pp. 412-417 ◽  
Author(s):  
Wing-On Ng ◽  
Rodolfo Zentella ◽  
Yinsheng Wang ◽  
John-Stephen A. Taylor ◽  
Himadri B. Pakrasi
Keyword(s):  
Pyrimidine Dimer ◽  
Cyclobutane Pyrimidine Dimer ◽  
Dna Photolyase ◽  
Synechocystis Sp ◽  
Pcc 6803

Mutagenesis in Escherichia coli : evidence for the mechanism of base change mutation by ultraviolet radiation in a strain deficient in excision-repair

1968 ◽  
Vol 171 (1023) ◽  
pp. 213-226 ◽  
Keyword(s):  
Escherichia Coli ◽  
Generation Time ◽  
Excision Repair ◽  
Indirect Evidence ◽  
Base Change ◽  
Pyrimidine Dimer ◽  
Mutagenic Action ◽  
Pyrimidine Dimers ◽  
Generation Times ◽  
Low Probability

The mutagenic action of u. v. radiation has been studied upon Escherichia coli WP2 try her growing exponentially at 37 °C. Although this strain is unable to excise pyrimidine dimers from its DNA it showed no detectable reduction in growth rate after exposure to a dose of u. v. (10 -6 J mm -2 ) calculated to produce several dozen pyrimidine dimers per chromosome. As judged by photoreversibility of mutations to prototrophy, dimers at mutable sites may persist for up to about 4 generation times after u. v. and may give rise to mutations with a low probability in each replication cycle during this period. The slow disappearance of dimers takes place whether or not DNA replication is inhibited and indirect evidence suggests that excision-repair may not be involved. Mutations are established (i. e. become non-photoreversible) only when DNA replication is taking place and are not expressible on unsupplemented medium until approximately one generation time after being established. It is suggested that the mutation is initially produced by the laying down of an incorrect base opposite a pyrimidine dimer at, or shortly after, replication; the mutation becomes transcribable only after a further replication gives rise to a duplex mutant in both strands. The observed segregation pattern strongly suggests that at this further replication the mutation is carried by both resulting daughter duplexes. This implies that the mutant strand initially produced opposite the dimer has a strong influence on the bases of both new strands laid down at the next replication.

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