Control of guanine-rich DNA secondary structures depending on the protease activity using a designed PNA peptide

2015 ◽  
Vol 13 (7) ◽  
pp. 2022-2025 ◽  
Author(s):  
Kenji Usui ◽  
Arisa Okada ◽  
Keita Kobayashi ◽  
Naoki Sugimoto
Keyword(s):  
Secondary Structure ◽  
Structure Formation ◽  
Protease Activity ◽  
Secondary Structures ◽  
Regulation System ◽  
Dna Secondary Structure ◽  
Secondary Structure Formation ◽  
Dna Secondary Structures

A regulation system for DNA secondary structure formation of G-rich sequences using a designed PNA peptide exhibiting an enzyme-responsive functionality, depending on the protease activity was constructed.

scholarly journals Alternative DNA secondary structure formation affects RNA polymerase II promoter-proximal pausing in human

2018 ◽  
Vol 19 (1) ◽  
Author(s):  
Karol Szlachta ◽  
Ryan G. Thys ◽  
Naomi D. Atkin ◽  
Levi C. T. Pierce ◽  
Stefan Bekiranov ◽  
...  
Keyword(s):  
Secondary Structure ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Structure Formation ◽  
Dna Secondary Structure ◽  
Secondary Structure Formation

scholarly journals DNA Secondary Structure Formation in Bacterial Gene Capture Systems at Single-Molecule Resolution

2014 ◽  
Vol 106 (2) ◽  
pp. 272a-273a
Author(s):  
Marko Swoboda ◽  
Maj Svea Grieb ◽  
Varsha Natarajan ◽  
Aleksandra Nivina ◽  
Didier Mazel ◽  
...  
Keyword(s):  
Secondary Structure ◽  
Structure Formation ◽  
Single Molecule ◽  
Dna Secondary Structure ◽  
Bacterial Gene ◽  
Gene Capture ◽  
Secondary Structure Formation

scholarly journals Non-canonical secondary structures arising from non-B-DNA motifs are determinants of mutagenesis

2017 ◽  
Author(s):  
Ilias Georgakopoulos-Soares ◽  
Sandro Morganella ◽  
Naman Jain ◽  
Martin Hemberg ◽  
Serena Nik-Zainal
Keyword(s):  
Secondary Structure ◽  
Structure Formation ◽  
Dna Sequences ◽  
Replication Timing ◽  
Secondary Structures ◽  
Reference Sequence ◽  
Secondary Structure Formation ◽  
Mutation Density ◽  
Recurrent Mutations ◽  
Time Domains

SummarySomatic mutations show variation in density across cancer genomes. Previous studies have shown that chromatin organization and replication time domains are correlated with and thus predictive of this variation 1,2,3,4,5. Here, we analyse 1,809 whole-genome sequences from nine cancer types 6,7,8 to show that a subset of repetitive DNA sequences called non-B motifs that predict non-canonical secondary structure formation 9,10,11,12 can independently account for variation in mutation density. However, combined with epigenetic factors and replication timing, the variance explained can be improved to 43-76%. Intriguingly, ~2-fold mutation enrichment is observed directly within non-B motifs, is focused on exposed structural components, and is dependent on physical properties that are optimal for secondary structure formation. Therefore, there is mounting evidence that secondary structures arising from non-B motifs are not simply associated with increased mutation density, they are possibly causally implicated. Our results suggest that they are determinants of mutagenesis and increase the likelihood of recurrent mutations in the genome 13,6. This analysis calls for caution in the interpretation of recurrent mutations and highlights the importance of taking non-B motifs, that can simply be inferred from the reference sequence, into consideration in background models of mutability henceforth.

scholarly journals Topoisomerase II contributes to DNA secondary structure-mediated double-stranded breaks

2020 ◽  
Vol 48 (12) ◽  
pp. 6654-6671
Author(s):  
Karol Szlachta ◽  
Arkadi Manukyan ◽  
Heather M Raimer ◽  
Sandeep Singh ◽  
Anita Salamon ◽  
...  
Keyword(s):  
Secondary Structure ◽  
Human Genome ◽  
Topoisomerase Ii ◽  
Genome Instability ◽  
Secondary Structures ◽  
Ctcf Binding ◽  
Dna Secondary Structure ◽  
Disease Etiology ◽  
Dna Secondary Structures ◽  
Genomic Regions

Abstract DNA double-stranded breaks (DSBs) trigger human genome instability, therefore identifying what factors contribute to DSB induction is critical for our understanding of human disease etiology. Using an unbiased, genome-wide approach, we found that genomic regions with the ability to form highly stable DNA secondary structures are enriched for endogenous DSBs in human cells. Human genomic regions predicted to form non-B-form DNA induced gross chromosomal rearrangements in yeast and displayed high indel frequency in human genomes. The extent of instability in both analyses is in concordance with the structure forming ability of these regions. We also observed an enrichment of DNA secondary structure-prone sites overlapping transcription start sites (TSSs) and CCCTC-binding factor (CTCF) binding sites, and uncovered an increase in DSBs at highly stable DNA secondary structure regions, in response to etoposide, an inhibitor of topoisomerase II (TOP2) re-ligation activity. Importantly, we found that TOP2 deficiency in both yeast and human leads to a significant reduction in DSBs at structure-prone loci, and that sites of TOP2 cleavage have a greater ability to form highly stable DNA secondary structures. This study reveals a direct role for TOP2 in generating secondary structure-mediated DNA fragility, advancing our understanding of mechanisms underlying human genome instability.

The Relationship Between Third-Codon Position Nucleotide Content, Codon Bias, mRNA Secondary Structure and Gene Expression in the Drosophilid Alcohol Dehydrogenase Genes Adh and Adhr

Genetics ◽  
2001 ◽  
Vol 159 (2) ◽  
pp. 623-633 ◽  
Author(s):  
David B Carlini ◽  
Ying Chen ◽  
Wolfgang Stephan
Keyword(s):  
Gene Expression ◽  
Secondary Structure ◽  
Structure Formation ◽  
Codon Bias ◽  
Codon Position ◽  
Secondary Structures ◽  
Structural Elements ◽  
Mrna Secondary Structure ◽  
Secondary Structure Formation ◽  
The Relationship

Abstract To gain insights into the relationship between codon bias, mRNA secondary structure, third-codon position nucleotide distribution, and gene expression, we predicted secondary structures in two related drosophilid genes, Adh and Adhr, which differ in degree of codon bias and level of gene expression. Individual structural elements (helices) were inferred using the comparative method. For each gene, four types of randomization simulations were performed to maintain/remove codon bias and/or to maintain or alter third-codon position nucleotide composition (N3). In the weakly expressed, weakly biased gene Adhr, the potential for secondary structure formation was found to be much stronger than in the highly expressed, highly biased gene Adh. This is consistent with the observation of approximately equal G and C percentages in Adhr (~31% across species), whereas in Adh the N3 distribution is shifted toward C (42% across species). Perturbing the N3 distribution to approximately equal amounts of A, G, C, and T increases the potential for secondary structure formation in Adh, but decreases it in Adhr. On the other hand, simulations that reduce codon bias without changing N3 content indicate that codon bias per se has only a weak effect on the formation of secondary structures. These results suggest that, for these two drosophilid genes, secondary structure is a relatively independent, negative regulator of gene expression. Whereas the degree of codon bias is positively correlated with level of gene expression, strong individual secondary structural elements may be selected for to retard mRNA translation and to decrease gene expression.

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