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Editorial Board Members’ Collection Series: Genome Stability

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 940

Special Issue Editors

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Guest Editor
Department of Biomedical Sciences, College of Natural Science, Dong-A University, Busan 49315, Republic of Korea
Interests: DNA damage; DNA repair; DNA replication; cell cycle checkpoint; circadian clock; nucleotide excision repair; ATR pathway
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Special Issue Information

Dear Colleagues,

The study of genome stability encompasses a broad spectrum of research areas, from genetics and molecular biology to biochemistry and bioinformatics. Its aim is to unravel the intricacies of genetic maintenance mechanisms, shedding light on their profound implications for health, notably in the realms of cancer, aging, and genetic disorders. The DNA damage response is a complex network of cellular mechanisms designed to detect, signal, and repair DNA lesions, playing a central role in maintaining genome stability by safeguarding the integrity of the genetic material. Unraveling the causes and consequences of genomic instability and its allied DNA damage response not only yields profound insights but also paves the way for targeted therapies and interventions.

Relevant topics for this collection may include the identification of novel genes associated with genome stability/instability, cutting-edge technologies for dissecting DNA damage response, and computational approaches for scrutinizing vast genomic datasets. Key focal points extend to DNA repair, replication, and recombination mechanisms, ATR/ATM checkpoint, and the impact of both internal and external genotoxins on genome stability.

Prof. Dr. Tae-Hong Kang
Prof. Dr. Lasse Lindahl
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.


  • genome stability
  • DNA damage response
  • DNA repair
  • DNA replication
  • DNA recombination
  • ATR/ATM pathway

Published Papers (1 paper)

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12 pages, 2511 KiB  
PCNA Unloading Is Crucial for the Bypass of DNA Lesions Using Homologous Recombination
by Matan Arbel-Groissman, Batia Liefshitz, Nir Katz, Maxim Kuryachiy and Martin Kupiec
Int. J. Mol. Sci. 2024, 25(6), 3359; https://doi.org/10.3390/ijms25063359 - 15 Mar 2024
Viewed by 664
DNA Damage Tolerance (DDT) mechanisms allow cells to bypass lesions in the DNA during replication. This allows the cells to progress normally through the cell cycle in the face of abnormalities in their DNA. PCNA, a homotrimeric sliding clamp complex, plays a central [...] Read more.
DNA Damage Tolerance (DDT) mechanisms allow cells to bypass lesions in the DNA during replication. This allows the cells to progress normally through the cell cycle in the face of abnormalities in their DNA. PCNA, a homotrimeric sliding clamp complex, plays a central role in the coordination of various processes during DNA replication, including the choice of mechanism used during DNA damage bypass. Mono-or poly-ubiquitination of PCNA facilitates an error-prone or an error-free bypass mechanism, respectively. In contrast, SUMOylation recruits the Srs2 helicase, which prevents local homologous recombination. The Elg1 RFC-like complex plays an important role in unloading PCNA from the chromatin. We analyze the interaction of mutations that destabilize PCNA with mutations in the Elg1 clamp unloader and the Srs2 helicase. Our results suggest that, in addition to its role as a coordinator of bypass mechanisms, the very presence of PCNA on the chromatin prevents homologous recombination, even in the absence of the Srs2 helicase. Thus, PCNA unloading seems to be a pre-requisite for recombinational repair. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Genome Stability)
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