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Genes
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DNA Damage and Repair in Microorganisms, Plants and Mammalian Systems
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DNA Damage and Repair in Microorganisms, Plants and Mammalian Systems

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

Deadline for manuscript submissions: 20 May 2024 | Viewed by 4274

Special Issue Editors

Prof. Dr. Ioly Kotta-Loizou

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Guest Editor
1. Department of Life Sciences, Faculty of Natural Sciences, Imperial College London, London, UK
2. Department of Clinical, Pharmaceutical and Biological Science, University of Hertfordshire, Hatfield AL10 9AB, UK
Interests: mycoviruses; mycovirus infection; mycovirus population studies; mycovirus evolution; mycovirus–fungus interactions; bacterial gene expression; RNA damage and repair; oxidative stress; antibiotics resistance; CRISPR-Cas
Special Issues, Collections and Topics in MDPI journals
Dr. Nan Zhang

E-Mail Website
Guest Editor
Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA
Interests: neurodegeneration; DNA damage repair; CRISPR-Cas; oligonucleotide therapy; mitochondrial dysfunction
Dr. Xin Wang

E-Mail Website
Guest Editor
Basic and Translational Research Division, Department of Cardiology, Boston Children’s Hospital, Harvard Medical School, Boston, MA 02115, USA
Interests: DNA double-strand break repair; templated insertion; ageing; cancer immunotherapy

Special Issue Information

Dear Colleagues,

Maitaining genome integrity is important for the perpetuation of all life forms. Cells that are constantly subject to endogenous and exogenous mutagens instigate robust DNA damage response (DDR), while persistent DNA damage triggers cell senescence or apoptosis. Mounting evidence suggests that the disruption and dysregulation of DNA damage repair play a key role in survival and adaptation of pathogens, cancer, neurodegeneration, and aging, to name but a few. DNA damage repair, in particular the p53 pathway, also contributes to the success and selection of CRISPR-based genome editing. In this Special Issue of Genes, we welcome reviews, research articles, brief communications, and perspectives that will employ biochemical and biophysical technologies to address the mechanisms of genotoxins, DDR pathways, telomere maintenance, DNA replication fidelity, repetitive sequences and chromosome fragility, and mitochondrial genome integrity in both microorganisms and mammalian systems. Therapeutic interventions, ranging from small molecules to biologics, that target DDR pathways in human diseases are also of special interest.

Dr. Ioly Kotta-Loizou
Dr. Nan Zhang
Dr. Xin Wang
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 and repair
  • genome instability
  • DNA replication
  • cancer
  • mitochondrial genome integrity
  • neurodegeneration

Published Papers (2 papers)

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17 pages, 4303 KiB  
Article
hMSH5 Regulates NHEJ and Averts Excessive Nucleotide Alterations at Repair Joints
by Aneesa T. Al-Soodani, Xiling Wu, Nicole C. Kelp, Alexander J. Brown, Steven A. Roberts and Chengtao Her
Genes 2022, 13(4), 673; https://doi.org/10.3390/genes13040673 - 11 Apr 2022
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Abstract
Inappropriate repair of DNA double-strand breaks (DSBs) leads to genomic instability, cell death, or malignant transformation. Cells minimize these detrimental effects by selectively activating suitable DSB repair pathways in accordance with their underlying cellular context. Here, we report that hMSH5 down-regulates NHEJ and [...] Read more.
Inappropriate repair of DNA double-strand breaks (DSBs) leads to genomic instability, cell death, or malignant transformation. Cells minimize these detrimental effects by selectively activating suitable DSB repair pathways in accordance with their underlying cellular context. Here, we report that hMSH5 down-regulates NHEJ and restricts the extent of DSB end processing before rejoining, thereby reducing “excessive” deletions and insertions at repair joints. RNAi-mediated knockdown of hMSH5 led to large nucleotide deletions and longer insertions at the repair joints, while at the same time reducing the average length of microhomology (MH) at repair joints. Conversely, hMSH5 overexpression reduced end-joining activity and increased RPA foci formation (i.e., more stable ssDNA at DSB ends). Furthermore, silencing of hMSH5 delayed 53BP1 chromatin spreading, leading to increased end resection at DSB ends. Full article
(This article belongs to the Special Issue DNA Damage and Repair in Microorganisms, Plants and Mammalian Systems)
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16 pages, 2688 KiB  
Brief Report
Dual Targeting of DNA Damage Response Proteins Implicated in Cancer Radioresistance
by Spyridon N. Vasilopoulos, Hüseyin Güner, Merve Uça Apaydın, Athanasia Pavlopoulou and Alexandros G. Georgakilas
Genes 2023, 14(12), 2227; https://doi.org/10.3390/genes14122227 - 17 Dec 2023
Viewed by 1114
Abstract
Ionizing radiation can induce different types of DNA lesions, leading to genomic instability and ultimately cell death. Radiation therapy or radiotherapy, a major modality in cancer treatment, harnesses the genotoxic potential of radiation to target and destroy cancer cells. Nevertheless, cancer cells have [...] Read more.
Ionizing radiation can induce different types of DNA lesions, leading to genomic instability and ultimately cell death. Radiation therapy or radiotherapy, a major modality in cancer treatment, harnesses the genotoxic potential of radiation to target and destroy cancer cells. Nevertheless, cancer cells have the capacity to develop resistance to radiation treatment (radioresistance), which poses a major obstacle in the effective management of cancer. It has been shown that administration of platinum-based drugs to cancer patients can increase tumor radiosensitivity, but despite this, it is associated with severe adverse effects. Several lines of evidence support that activation of the DNA damage response and repair machinery in the irradiated cancer cells enhances radioresistance and cellular survival through the efficient repair of DNA lesions. Therefore, targeting of key DNA damage repair factors would render cancer cells vulnerable to the irradiation effects, increase cancer cell killing, and reduce the risk of side effects on healthy tissue. Herein, we have employed a computer-aided drug design approach for generating ab initio a chemical compound with drug-like properties potentially targeting two proteins implicated in multiple DNA repair pathways. The findings of this study could be taken into consideration in clinical decision-making in terms of co-administering radiation with DNA damage repair factor-based drugs. Full article
(This article belongs to the Special Issue DNA Damage and Repair in Microorganisms, Plants and Mammalian Systems)
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