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Editorial Board Members’ Collection Series: Genome Stability
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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: 20 September 2025 | Viewed by 9885

Special Issue Editors

Prof. Dr. Tae-Hong Kang

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Lasse Lindahl

E-Mail Website
Guest Editor
Department of Biological Sciences, University of Maryland Baltimore County, Baltimore, MD 21250, USA
Interests: ribosome formation and function; RNA processing; protein-RNA complexes
Special Issues, Collections and Topics in MDPI journals

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.

Keywords

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

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Published Papers (5 papers)

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Research

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14 pages, 5206 KiB  
Article
Base Excision Repair in Mitotic Cells and the Role of Apurinic/Apyrimidinic Endonuclease 1 (APE1) in Post-Mitotic Transcriptional Reactivation of Genes
by Suravi Pramanik, Yingling Chen and Kishor K. Bhakat
Int. J. Mol. Sci. 2024, 25(23), 12735; https://doi.org/10.3390/ijms252312735 - 27 Nov 2024
Viewed by 1047
Abstract
Endogenous DNA damage occurs throughout the cell cycle, with cells responding differently at various stages. The base excision repair (BER) pathway predominantly repairs damaged bases in the genome. While extensively studied in interphase cells, it is unknown if BER operates in mitosis and [...] Read more.
Endogenous DNA damage occurs throughout the cell cycle, with cells responding differently at various stages. The base excision repair (BER) pathway predominantly repairs damaged bases in the genome. While extensively studied in interphase cells, it is unknown if BER operates in mitosis and how apurinic/apyrimidinic (AP) sites, intermediates in the BER pathway that inhibit transcriptional elongation, are processed for post-mitotic gene reactivation. In this study, using an alkaline comet assay, we demonstrate that BER is inefficient in mitosis and that AP endonuclease 1 (APE1), a key BER enzyme, is required for the repair of damage post-mitosis. We previously demonstrated that APE1 is acetylated (AcAPE1) in the chromatin. Using high-resolution microscopy, we show that AcAPE1 remains associated with specific regions in the condensed chromatin in each of the phases of mitosis. This association presumably occurs via the binding of APE1 to the G-quadruplex structure, a non-canonical DNA structure predominantly present in the transcribed gene regions. Additionally, using a nascent RNA detection strategy, we demonstrate that the knockdown of APE1 delayed the rapid post-mitotic transcriptional reactivation of genes. Our findings highlight the functional importance of APE1 in the mitotic chromosomes to facilitate faster repair of endogenous damage and rapid post-mitotic gene reactivation in daughter cells. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Genome Stability)
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12 pages, 2511 KiB  
Article
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
Cited by 1 | Viewed by 1718
Abstract
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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Review

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20 pages, 2222 KiB  
Review
Transcription-Coupled Repair and R-Loop Crosstalk in Genome Stability
by Jeseok Jeon and Tae-Hong Kang
Int. J. Mol. Sci. 2025, 26(8), 3744; https://doi.org/10.3390/ijms26083744 - 16 Apr 2025
Viewed by 230
Abstract
Transcription-coupled repair (TCR) and R-loops are two interrelated processes critical to the maintenance of genome stability during transcription. TCR, a specialized sub-pathway of nucleotide excision repair, rapidly removes transcription-blocking lesions from the transcribed strand of active genes, thereby safeguarding transcription fidelity and cellular [...] Read more.
Transcription-coupled repair (TCR) and R-loops are two interrelated processes critical to the maintenance of genome stability during transcription. TCR, a specialized sub-pathway of nucleotide excision repair, rapidly removes transcription-blocking lesions from the transcribed strand of active genes, thereby safeguarding transcription fidelity and cellular homeostasis. In contrast, R-loops, RNA–DNA hybrid structures formed co-transcriptionally, play not only regulatory roles in gene expression and replication but can also contribute to genome instability when persistently accumulated. Recent experimental evidence has revealed dynamic crosstalk between TCR and R-loop resolution pathways. This review highlights current molecular and cellular insights into TCR and R-loop biology, discusses the impact of their crosstalk, and explores emerging therapeutic strategies aimed at optimizing DNA repair and reducing disease risk in conditions such as cancer and neurodegenerative disorders. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Genome Stability)
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17 pages, 2056 KiB  
Review
Helicase HELQ: Molecular Characters Fit for DSB Repair Function
by Yuqin Zhao, Kaiping Hou, Yu Liu, Yinan Na, Chao Li, Haoyuan Luo and Hailong Wang
Int. J. Mol. Sci. 2024, 25(16), 8634; https://doi.org/10.3390/ijms25168634 - 8 Aug 2024
Viewed by 1521
Abstract
The protein sequence and spatial structure of DNA helicase HELQ are highly conserved, spanning from archaea to humans. Aside from its helicase activity, which is based on DNA binding and translocation, it has also been recently reconfirmed that human HELQ possesses DNA–strand–annealing activity, [...] Read more.
The protein sequence and spatial structure of DNA helicase HELQ are highly conserved, spanning from archaea to humans. Aside from its helicase activity, which is based on DNA binding and translocation, it has also been recently reconfirmed that human HELQ possesses DNA–strand–annealing activity, similar to that of the archaeal HELQ homolog StoHjm. These biochemical functions play an important role in regulating various double–strand break (DSB) repair pathways, as well as multiple steps in different DSB repair processes. HELQ primarily facilitates repair in end–resection–dependent DSB repair pathways, such as homologous recombination (HR), single–strand annealing (SSA), microhomology–mediated end joining (MMEJ), as well as the sub-pathways’ synthesis–dependent strand annealing (SDSA) and break–induced replication (BIR) within HR. The biochemical functions of HELQ are significant in end resection and its downstream pathways, such as strand invasion, DNA synthesis, and gene conversion. Different biochemical activities are required to support DSB repair at various stages. This review focuses on the functional studies of the biochemical roles of HELQ during different stages of diverse DSB repair pathways. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Genome Stability)
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21 pages, 4560 KiB  
Review
Cosmic Ionizing Radiation: A DNA Damaging Agent That May Underly Excess Cancer in Flight Crews
by Sneh M. Toprani, Christopher Scheibler, Irina Mordukhovich, Eileen McNeely and Zachary D. Nagel
Int. J. Mol. Sci. 2024, 25(14), 7670; https://doi.org/10.3390/ijms25147670 - 12 Jul 2024
Cited by 4 | Viewed by 4393
Abstract
In the United States, the Federal Aviation Administration has officially classified flight crews (FC) consisting of commercial pilots, cabin crew, or flight attendants as “radiation workers” since 1994 due to the potential for cosmic ionizing radiation (CIR) exposure at cruising altitudes originating from [...] Read more.
In the United States, the Federal Aviation Administration has officially classified flight crews (FC) consisting of commercial pilots, cabin crew, or flight attendants as “radiation workers” since 1994 due to the potential for cosmic ionizing radiation (CIR) exposure at cruising altitudes originating from solar activity and galactic sources. Several epidemiological studies have documented elevated incidence and mortality for several cancers in FC, but it has not yet been possible to establish whether this is attributable to CIR. CIR and its constituents are known to cause a myriad of DNA lesions, which can lead to carcinogenesis unless DNA repair mechanisms remove them. But critical knowledge gaps exist with regard to the dosimetry of CIR, the role of other genotoxic exposures among FC, and whether possible biological mechanisms underlying higher cancer rates observed in FC exist. This review summarizes our understanding of the role of DNA damage and repair responses relevant to exposure to CIR in FC. We aimed to stimulate new research directions and provide information that will be useful for guiding regulatory, public health, and medical decision-making to protect and mitigate the risks for those who travel by air. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Genome Stability)
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