Promotion of Single-Strand Invasion of PNA to Double-Stranded DNA by Pseudo-Complementary Base Pairing

2019 ◽  
Vol 92 (2) ◽  
pp. 330-335 ◽  
Author(s):  
Narumi Shigi ◽  
Yuki Mizuno ◽  
Hiroko Kunifuda ◽  
Kazunari Matsumura ◽  
Makoto Komiyama
Keyword(s):  
Single Strand ◽  
Base Pairing ◽  
Double Stranded Dna ◽  
Strand Invasion

scholarly journals Cooperative strand invasion of double-stranded DNA by peptide nucleic acid

2005 ◽  
Vol 49 (1) ◽  
pp. 167-168 ◽  
Author(s):  
Toru Sugiyama ◽  
Yasutada Imamura ◽  
Wataru Hakamata ◽  
Masaaki Kurihara ◽  
Atsushi Kittaka
Keyword(s):  
Nucleic Acid ◽  
Peptide Nucleic Acid ◽  
Double Stranded Dna ◽  
Strand Invasion

scholarly journals Monitoring the Transcriptional Activity of Human Endogenous Retroviral HERV-W Family Using PNA Strand Invasion into Double-Stranded DNA

2018 ◽  
Vol 60 (2) ◽  
pp. 124-133 ◽  
Author(s):  
Grzegorz Machnik ◽  
Estera Skudrzyk ◽  
Łukasz Bułdak ◽  
Jarosław Ruczyński ◽  
Agnieszka Kozłowska ◽  
...  
Keyword(s):  
Transcriptional Activity ◽  
Double Stranded Dna ◽  
Strand Invasion

scholarly journals Sequence-specific recognition of double-stranded DNA by cooperative strand invasion

2006 ◽  
Vol 50 (1) ◽  
pp. 157-158
Author(s):  
Toru Sugiyama ◽  
Yasutada Imamura ◽  
Wataru Hakamata ◽  
Masaaki Kurihara ◽  
Atsushi Kittaka
Keyword(s):  
Specific Recognition ◽  
Double Stranded Dna ◽  
Strand Invasion

scholarly journals Conservative Repair of a Chromosomal Double-Strand Break by Single-Strand DNA through Two Steps of Annealing

2006 ◽  
Vol 26 (20) ◽  
pp. 7645-7657 ◽  
Author(s):  
Francesca Storici ◽  
Joyce R. Snipe ◽  
Godwin K. Chan ◽  
Dmitry A. Gordenin ◽  
Michael A. Resnick
Keyword(s):  
Normal Cell ◽  
Strand Break ◽  
Double Strand Breaks ◽  
Single Strand ◽  
Dsb Repair ◽  
Strand Breaks ◽  
Single Strand Annealing ◽  
Repair Mechanisms ◽  
Strand Invasion ◽  
Strand Annealing

ABSTRACT The repair of chromosomal double-strand breaks (DSBs) is essential to normal cell growth, and homologous recombination is a universal process for DSB repair. We explored DSB repair mechanisms in the yeast Saccharomyces cerevisiae using single-strand oligonucleotides with homology to both sides of a DSB. Oligonucleotide-directed repair occurred exclusively via Rad52- and Rad59-mediated single-strand annealing (SSA). Even the SSA domain of human Rad52 provided partial complementation for a null rad52 mutation. The repair did not involve Rad51-driven strand invasion, and moreover the suppression of strand invasion increased repair with oligonucleotides. A DSB was shown to activate targeting by oligonucleotides homologous to only one side of the break at large distances (at least 20 kb) from the break in a strand-biased manner, suggesting extensive 5′ to 3′ resection, followed by the restoration of resected DNA to the double-strand state. We conclude that long resected chromosomal DSB ends are repaired by a single-strand DNA oligonucleotide through two rounds of annealing. The repair by single-strand DNA can be conservative and may allow for accurate restoration of chromosomal DNAs with closely spaced DSBs.

scholarly journals Methoxyamine attack on cytosine produces ambivalent base pairing properties of the modified base.

1996 ◽  
Vol 43 (1) ◽  
pp. 95-105 ◽  
Author(s):  
Z Gdaniec ◽  
L C Sowers ◽  
G V Fazakerley
Keyword(s):  
Low Temperature ◽  
Methoxy Group ◽  
Solution Structure ◽  
Pair Formation ◽  
Single Strand ◽  
The Other ◽  
Base Pairing ◽  
Slow Exchange ◽  
Amino Form ◽  
Opposite Strand

We report the solution structure of two heptanucleotides each containing a central N4-methoxycytosine, in one case with adenine on the opposite strand and in the other with guanine. For the N4-methoxycytosine-adenine pair only the imino form of the N4-methoxycytosine residue is observed and base pairing is in Watson-Crick geometry. However, rotation of the methoxy group about the N-OCH3 bond is not constrained to a particular orientation although it must be anti to the N3 of N4-methoxycytosine. The slow exchange on a proton NMR time scale between the single strand and double strand forms is attributed to the strong preference of the syn conformation of the OCH3 group in the single strand which inhibits base pair formation. For N4-methoxycytosine base paired with guanosine we observe the N4-methoxycytosine base in the amino form in Watson-Crick geometry and a slow exchange of this species with an imino form base paired in wobble geometry. The amino form is predominant at low temperature whereas the imino form predominates above 40 degrees C. Our results point to preferential replacement of dTTP by N4-methoxycytosine in primer elongation.

scholarly journals Single-strand specific nuclease enhances accuracy of error-corrected sequencing and improves rare mutation-detection sensitivity

2021 ◽  
Author(s):  
Yuki Otsubo ◽  
Shoji Matsumura ◽  
Naohiro Ikeda ◽  
Masayuki Yamane
Keyword(s):  
Dna Sequences ◽  
Mutation Detection ◽  
Single Strand ◽  
Detection Sensitivity ◽  
Induced Mutations ◽  
Mung Bean Nuclease ◽  
S1 Nuclease ◽  
Rare Mutation ◽  
Rare Mutations ◽  
Double Stranded Dna

AbstractError-corrected sequences (ECSs) that utilize double-stranded DNA sequences are useful in detecting mutagen-induced mutations. However, relatively higher frequencies of G:C > T:A (1 × 10−7 bp) and G:C > C:G (2 × 10−7 bp) errors decrease the accuracy of detection of rare G:C mutations (approximately 10−7 bp). Oxidized guanines in single-strand (SS) overhangs generated after shearing could serve as the source of these errors. To remove these errors, we first computationally discarded up to 20 read bases corresponding to the ends of the DNA fragments. Error frequencies decreased proportionately with trimming length; however, the results indicated that they were not sufficiently removed. To efficiently remove SS overhangs, we evaluated three mechanistically distinct SS-specific nucleases (S1 Nuclease, mung bean nuclease, and RecJf exonuclease) and found that they were more efficient than computational trimming. Consequently, we established Jade-Seq™, an ECS protocol with S1 Nuclease treatment, which reduced G:C > T:A and G:C > C:G errors to 0.50 × 10−7 bp and 0.12 × 10−7 bp, respectively. This was probably because S1 Nuclease removed SS regions, such as gaps and nicks, depending on its wide substrate specificity. Subsequently, we evaluated the mutation-detection sensitivity of Jade-Seq™ using DNA samples from TA100 cells exposed to 3-methylcholanthrene and 7,12-dimethylbenz[a]anthracene, which contained the rare G:C > T:A mutation (i.e., 2 × 10−7 bp). Fold changes of G:C > T:A compared to the vehicle control were 1.2- and 1.3-times higher than those of samples without S1 Nuclease treatment, respectively. These findings indicate the potential of Jade-Seq™ for detecting rare mutations and determining the mutagenicity of environmental mutagens.

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