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Special Issue "DNA Damage Response (DDR) and DNA Repair"

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 January 2022.

Special Issue Editor

Dr. Fiammetta Verni
E-Mail Website
Guest Editor
Department Biology and Biotechnology "Charles Darwin", Sapienza University of Rome, Rome, Italy
Interests: genetics; chromosome structure and segregation; DNA repair; cell division

Special Issue Information

Dear Colleagues,

A large body of evidence indicates that DNA alterations such as chromosome aberrations and mutations can lead to several diseases, including cancer, and affect some aspects of aging. Each cell in the human body receives tens of thousands of DNA lesions per day that threaten the integrity of the genome. DNA lesions include base oxidation or alkylation, mismatch of nucleotides, crosslinks between intra- or inter- DNA strands, and single or double DNA strand breaks. Cells have evolved several mechanisms to counteract these various types of DNA damage, the importance of which is emphasized by the fact that mutations in genes required for DNA damage response (DDR) and DNA repair can result in genetic disorders, genomic instability, or cancer predisposition. In addition to radiations (i.e., UV light, X-rays) or chemicals, endogenous processes of oxidative stress and inflammation also cause DNA damage. Furthermore, there is accumulating evidence on how diet can have an impact on DNA and, ultimately, on cancer. The deficiency of micronutrients such as minerals and vitamins—which work as cofactors of enzymes involved in DNA metabolism— has been shown to cause single- and double-strand breaks, oxidative lesions, or both. Moreover, micronutrients can influence DNA folding and remodeling, an essential part of accurate double-strand break repair.

Although a significant number of studies concerning all these topics have been published over the past several decades. more investigation is required to reach a deeper understanding of the underlying molecular mechanisms. In this Special Issue, we aim to offer a comprehensive overview of the current understanding of mechanisms at the basis of DNA integrity maintenance and explore how the impairment of these mechanisms can lead to human diseases such as cancer or neurodegenerative diseases. 

This Special Issue invites original studies and review articles covering the following themes:

  1. Mechanisms at the basis of DDR and DNA repair;
  2. Biological consequences of deficiency in DDR and DNA repair;
  3. Maintenance of genome stability;
  4. Relationship between metabolism and DNA damage;
  5. How chromatin structure influences repair processes;
  6. Perspective or preclinical implications of genome instability in genetic disorders, neurodegenerative diseases, and cancer using cells and animal models.

Dr. Fiammetta Verni
Guest Editor

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 papers will be 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.


  • DDR
  • DNA repair
  • genome stability

Published Papers (1 paper)

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The Cdc14 Phosphatase Controls Resolution of Recombination Intermediates and Crossover Formation during Meiosis
Int. J. Mol. Sci. 2021, 22(18), 9811; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22189811 - 10 Sep 2021
Cited by 1 | Viewed by 608
Meiotic defects derived from incorrect DNA repair during gametogenesis can lead to mutations, aneuploidies and infertility. The coordinated resolution of meiotic recombination intermediates is required for crossover formation, ultimately necessary for the accurate completion of both rounds of chromosome segregation. Numerous master kinases [...] Read more.
Meiotic defects derived from incorrect DNA repair during gametogenesis can lead to mutations, aneuploidies and infertility. The coordinated resolution of meiotic recombination intermediates is required for crossover formation, ultimately necessary for the accurate completion of both rounds of chromosome segregation. Numerous master kinases orchestrate the correct assembly and activity of the repair machinery. Although much less is known, the reversal of phosphorylation events in meiosis must also be key to coordinate the timing and functionality of repair enzymes. Cdc14 is a crucial phosphatase required for the dephosphorylation of multiple CDK1 targets in many eukaryotes. Mutations that inactivate this phosphatase lead to meiotic failure, but until now it was unknown if Cdc14 plays a direct role in meiotic recombination. Here, we show that the elimination of Cdc14 leads to severe defects in the processing and resolution of recombination intermediates, causing a drastic depletion in crossovers when other repair pathways are compromised. We also show that Cdc14 is required for the correct activity and localization of the Holliday Junction resolvase Yen1/GEN1. We reveal that Cdc14 regulates Yen1 activity from meiosis I onwards, and this function is essential for crossover resolution in the absence of other repair pathways. We also demonstrate that Cdc14 and Yen1 are required to safeguard sister chromatid segregation during the second meiotic division, a late action that is independent of the earlier role in crossover formation. Thus, this work uncovers previously undescribed functions of the evolutionary conserved Cdc14 phosphatase in the regulation of meiotic recombination. Full article
(This article belongs to the Special Issue DNA Damage Response (DDR) and DNA Repair)
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