Deformable nature of various damaged DNA duplexes estimated by an electrochemical analysis on electrodes

Chiba, Junya; Aoki, Shun; Yamamoto, Junpei; Iwai, Shigenori; Inoûye, Masahiko

doi:10.1039/c4cc04513k

Cited by 3 publications

(3 citation statements)

References 29 publications

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“…The 23-bp oligonucleotide presents a locally narrower minor groove in correspondence of the AP sites due to the B helix compression subsequent to the ejection of the lesions, but no marked deviation of the backbone. In contrast, backbone deformation leading to bulge have been observed in the case of single AP site and extensively studied ( 42 – 45 ). The absence of bulge is an important feature that one can relate to the lack of repair of seq0: the duplex structural reorganization, acts as such to make the damaged oligonucleotide extremely close to a non-damaged 22-bp B-DNA strand with, in its center, two dangling extrahelical AP sites.…”

Section: Resultsmentioning

confidence: 99%

Correlation of bistranded clustered abasic DNA lesion processing with structural and dynamic DNA helix distortion

et al. 2016

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Clustered apurinic/apyrimidinic (AP; abasic) DNA lesions produced by ionizing radiation are by far more cytotoxic than isolated AP lesion entities. The structure and dynamics of a series of seven 23-bp oligonucleotides featuring simple bistranded clustered damage sites, comprising of two AP sites, zero, one, three or five bases 3′ or 5′ apart from each other, were investigated through 400 ns explicit solvent molecular dynamics simulations. They provide representative structures of synthetically engineered multiply damage sites-containing oligonucleotides whose repair was investigated experimentally (Nucl. Acids Res. 2004, 32:5609-5620; Nucl. Acids Res. 2002, 30: 2800–2808). The inspection of extrahelical positioning of the AP sites, bulge and non Watson–Crick hydrogen bonding corroborates the experimental measurements of repair efficiencies by bacterial or human AP endonucleases Nfo and APE1, respectively. This study provides unprecedented knowledge into the structure and dynamics of clustered abasic DNA lesions, notably rationalizing the non-symmetry with respect to 3′ to 5′ position. In addition, it provides strong mechanistic insights and basis for future studies on the effects of clustered DNA damage on the recognition and processing of these lesions by bacterial or human DNA repair enzymes specialized in the processing of such lesions.

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Section: Resultsmentioning

confidence: 99%

Correlation of bistranded clustered abasic DNA lesion processing with structural and dynamic DNA helix distortion

et al. 2016

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“…3E , 5E , and 7A , Table 1 ). Recently, Chiba et al reported that their electrochemical analysis demonstrated the helix bending in duplexes containing several types of DNA lesions including the same abasic site analog [ 38 ]. Their study supports the idea that the disulfide bond was formed depending on the helix bending in our study.…”

Section: Discussionmentioning

confidence: 99%

“…However, the bent structure is the major conformation of bulged duplexes, and thus these methods are not suitable for the analysis of the bendability of abasic site-containing duplexes, which are expected to have an average structure similar to that of undamaged DNA. We recently collaborated with a research group in the field of electrochemistry to analyze the helix bending in damaged DNA [ 38 ], but static and dynamic bends could not be distinguished. In this article, we describe a method to detect helix bending in DNA, using the formation of a disulfide bond between two mercaptoalkyl groups attached to positions facing each other across the major groove in a duplex, as shown in Fig.…”

Section: Introductionmentioning

confidence: 99%

Analysis of Structural Flexibility of Damaged DNA Using Thiol-Tethered Oligonucleotide Duplexes

et al. 2015

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Bent structures are formed in DNA by the binding of small molecules or proteins. We developed a chemical method to detect bent DNA structures. Oligonucleotide duplexes in which two mercaptoalkyl groups were attached to the positions facing each other across the major groove were prepared. When the duplex contained the cisplatin adduct, which was proved to induce static helix bending, interstrand disulfide bond formation under an oxygen atmosphere was detected by HPLC analyses, but not in the non-adducted duplex, when the two thiol-tethered nucleosides were separated by six base pairs. When the insert was five and seven base pairs, the disulfide bond was formed and was not formed, respectively, regardless of the cisplatin adduct formation. The same reaction was observed in the duplexes containing an abasic site analog and the (6–4) photoproduct. Compared with the cisplatin case, the disulfide bond formation was slower in these duplexes, but the reaction rate was nearly independent of the linker length. These results indicate that dynamic structural changes of the abasic site- and (6–4) photoproduct-containing duplexes could be detected by our method. It is strongly suggested that the UV-damaged DNA-binding protein, which specifically binds these duplexes and functions at the first step of global-genome nucleotide excision repair, recognizes the easily bendable nature of damaged DNA.

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First paraben substituted cyclotetraphosphazene compounds and DNA interaction analysis with a new automated biosensor

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et al. 2016

Biosensors and Bioelectronics

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Deformable nature of various damaged DNA duplexes estimated by an electrochemical analysis on electrodes

Cited by 3 publications

References 29 publications

Correlation of bistranded clustered abasic DNA lesion processing with structural and dynamic DNA helix distortion

Correlation of bistranded clustered abasic DNA lesion processing with structural and dynamic DNA helix distortion

Analysis of Structural Flexibility of Damaged DNA Using Thiol-Tethered Oligonucleotide Duplexes

First paraben substituted cyclotetraphosphazene compounds and DNA interaction analysis with a new automated biosensor

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