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Mechanisms of DNA Damage, Repair and Mutagenesis 2023
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Mechanisms of DNA Damage, Repair and Mutagenesis 2023

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (25 October 2023) | Viewed by 3286

Special Issue Editors

Prof. Dr. Martin Kupiec

E-Mail Website
Guest Editor
The Shmunis School of Biomedicine & Cancer Research, Tel Aviv University, Ramat Aviv, Tel Aviv 69978, Israel
Interests: Saccharomyces cerevisiae; Schizosaccharomyces pombe; yeast; genome stability; DNA repair; telomeres
Special Issues, Collections and Topics in MDPI journals
Dr. Maciej Wnuk

E-Mail Website
Guest Editor
Department of Biotechnology, University of Rzeszow, Pigonia 1 A0, 35-310 Rzeszow, Poland
Interests: cancer cells; yeast cell biology; chromosomes; genomic instability; senescence; toxicology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

It is well known that DNA damage may affect the development and differentiation process in all living organisms leading to death, increased cellular heterogeneity, premature senescence, or uncontrolled, abnormal growth of cells. The stability of the genome is strictly related to the activity of mechanisms able to detect and repair DNA breaks, damaged or incompletely replicated DNA, or DNA sequence mismatches and mutation. In this Special Issue of Genes, we welcome reviews, new methods, original research articles, and communications that advance our understanding of all aspects of mechanisms of DNA damage, repair, and mutagenesis from evolutionary aspects to biological, medical, and biotechnological implications. While the mechanisms involved in the maintenance of telomere—rDNA, centromere, and heterochromatin—will be of special interest, we are open to any advancement exploring the genome structural variation and chromosomal aberrations, including aneuploidy as well as molecular epidemiology and mechanisms of genotoxicity.

Prof. Dr. Martin Kupiec
Dr. Maciej Wnuk
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

 

Keywords

  • DNA damage
  • DNA repair
  • mutagenesis
  • genomic instability
  • chromosome maintenance
  • DNA replication
  • DNA damage checkpoint

Published Papers (2 papers)

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Research

17 pages, 1062 KiB  
Article
Homologous Recombination and Repair Functions Required for Mutagenicity during Yeast Meiosis
by Liat Morciano, Renana M. Elgrabli, Drora Zenvirth and Ayelet Arbel-Eden
Genes 2023, 14(11), 2017; https://doi.org/10.3390/genes14112017 - 28 Oct 2023
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Abstract
Several meiotic events reshape the genome prior to its transfer (via gametes) to the next generation. The occurrence of new meiotic mutations is tightly linked to homologous recombination (HR) and firmly depends on Spo11-induced DNA breaks. To gain insight into the molecular mechanisms [...] Read more.
Several meiotic events reshape the genome prior to its transfer (via gametes) to the next generation. The occurrence of new meiotic mutations is tightly linked to homologous recombination (HR) and firmly depends on Spo11-induced DNA breaks. To gain insight into the molecular mechanisms governing mutagenicity during meiosis, we examined the timing of mutation and recombination events in cells deficient in various DNA HR-repair genes, which represent distinct functions along the meiotic recombination process. Despite sequence similarities and overlapping activities of the two DNA translocases, Rad54 and Tid1, we observed essential differences in their roles in meiotic mutation occurrence: in the absence of Rad54, meiotic mutagenicity was elevated 8-fold compared to the wild type (WT), while in the tid1Δ mutant, there were few meiotic mutations, nine percent compared to the WT. We propose that the presence of Rad54 channels recombinational repair to a less mutagenic pathway, whereas repair assisted by Tid1 is more mutagenic. A 3.5-fold increase in mutation level was observed in dmc1∆ cells, suggesting that single-stranded DNA (ssDNA) may be a potential source for mutagenicity during meiosis. Taken together, we suggest that the introduction of de novo mutations also contributes to the diversification role of meiotic recombination. These rare meiotic mutations revise genomic sequences and may contribute to long-term evolutionary changes. Full article
(This article belongs to the Special Issue Mechanisms of DNA Damage, Repair and Mutagenesis 2023)
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14 pages, 1888 KiB  
Article
A Role for the Interactions between Polδ and PCNA Revealed by Analysis of pol3-01 Yeast Mutants
by Shaked Nir Heyman, Mika Golan, Batia Liefshitz and Martin Kupiec
Genes 2023, 14(2), 391; https://doi.org/10.3390/genes14020391 - 02 Feb 2023
Viewed by 1686
Abstract
Several DNA polymerases participate in DNA synthesis during genome replication and DNA repair. PCNA, a homotrimeric ring, acts as a processivity factor for DNA polymerases. PCNA also acts as a “landing pad” for proteins that interact with chromatin and DNA at the moving [...] Read more.
Several DNA polymerases participate in DNA synthesis during genome replication and DNA repair. PCNA, a homotrimeric ring, acts as a processivity factor for DNA polymerases. PCNA also acts as a “landing pad” for proteins that interact with chromatin and DNA at the moving fork. The interaction between PCNA and polymerase delta (Polδ) is mediated by PIPs (PCNA-interacting peptides), in particular the one on Pol32, a regulatory subunit of Polδ. Here, we demonstrate that pol3-01, an exonuclease mutant of Polδ’s catalytic subunit, exhibits a weak interaction with Pol30 compared to the WT DNA polymerase. The weak interaction activates DNA bypass pathways, leading to increased mutagenesis and sister chromatid recombination. Strengthening pol3-01′s weak interaction with PCNA suppresses most of the phenotypes. Our results are consistent with a model in which Pol3-01 tends to detach from the chromatin, allowing an easier replacement of Polδ by the trans-lesion synthesis polymerase Zeta (Polz), thus leading to the increased mutagenic phenotype. Full article
(This article belongs to the Special Issue Mechanisms of DNA Damage, Repair and Mutagenesis 2023)
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