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Latest Progress in DNA Damage and DNA Repair
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Latest Progress in DNA Damage 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: closed (29 July 2024) | Viewed by 4749

Special Issue Editors

Dr. Mahara Valverde

E-Mail Website
Guest Editor
Departamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad Universitaria, Mexico City 04510, Mexico
Interests: DNA damage as early-disease biomarker; DNA repair and DDR in cell differentiation; DNA functionality in exposed human populations
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Emilio Rojas

E-Mail Website
Guest Editor
Departamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad Universitaria, Mexico City 04510, Mexico
Interests: xenobiotic-associated DNA damage; the post-transcriptional regulation of DNA repair; DNA repair; chemoresistance

Special Issue Information

Dear Colleagues,

DNA damage is the product of endless endogenous and exogenous insults that can induce alterations that compromise gene integrity, depending on the efficiency of DNA repair mechanisms. The molecular, biochemical, and cellular consequences of the great diversity of lesions that DNA can suffer from are still the subject of study due to its versatile response through mechanisms to safeguard the integrity of the genome (DNA repair), as part of the physiological responses that maintain homeostasis, until leading to the acquisition of mutations and/or diseases of a different nature.

This Special Issue, titled "Latest Progress in DNA Damage and DNA Repair", aims to present new tools that allow the study of DNA damage and DNA repair mechanisms through the use of different study models.

Recently, the area has diversified significantly and comprises different facets, including basic science, experimental cellular and molecular biology, and applied science, which are necessary in order to propose and promote therapeutic alternatives.

Dr. Mahara Valverde
Prof. Dr. Emilio Rojas
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

  • DNA damage
  • DNA repair mechanisms
  • DNA damage response (DDR)
  • post-translational regulation
  • chemoresistance
  • cell diferentiation
  • disease

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Published Papers (3 papers)

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Research

20 pages, 17046 KiB  
Article
CDC20 Holds Novel Regulation Mechanism in RPA1 during Different Stages of DNA Damage to Induce Radio-Chemoresistance
by Yang Gao, Pengbo Wen, Chenran Shao, Cheng Ye, Yuji Chen, Junyu You and Zhongjing Su
Int. J. Mol. Sci. 2024, 25(15), 8383; https://doi.org/10.3390/ijms25158383 - 1 Aug 2024
Viewed by 910
Abstract
Targeting CDC20 can enhance the radiosensitivity of tumor cells, but the function and mechanism of CDC20 on DNA damage repair response remains vague. To examine that issue, tumor cell lines, including KYSE200, KYSE450, and HCT116, were utilized to detect the expression, function, and [...] Read more.
Targeting CDC20 can enhance the radiosensitivity of tumor cells, but the function and mechanism of CDC20 on DNA damage repair response remains vague. To examine that issue, tumor cell lines, including KYSE200, KYSE450, and HCT116, were utilized to detect the expression, function, and underlying mechanism of CDC20 in radio-chemoresistance. Western blot and immunofluorescence staining were employed to confirm CDC20 expression and location, and radiation could upregulate the expression of CDC20 in the cell nucleus. The homologous recombination (HR) and non-homologous end joining (NHEJ) reporter gene systems were utilized to explore the impact of CDC20 on DNA damage repair, indicating that CDC20 could promote HR repair and radio/chemo-resistance. In the early stages of DNA damage, CDC20 stabilizes the RPA1 protein through protein-protein interactions, activating the ATR-mediated signaling cascade, thereby aiding in genomic repair. In the later stages, CDC20 assists in the subsequent steps of damage repair by the ubiquitin-mediated degradation of RPA1. CCK-8 and colony formation assay were used to detect the function of CDC20 in cell vitality and proliferation, and targeting CDC20 can exacerbate the increase in DNA damage levels caused by cisplatin or etoposide. A tumor xenograft model was conducted in BALB/c-nu/nu mice to confirm the function of CDC20 in vivo, confirming the in vitro results. In conclusion, this study provides further validation of the potential clinical significance of CDC20 as a strategy to overcome radio-chemoresistance via uncovering a novel role of CDC20 in regulating RPA1 during DNA damage repair. Full article
(This article belongs to the Special Issue Latest Progress in DNA Damage and DNA Repair)
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15 pages, 2515 KiB  
Article
Modification of Seurat v4 for the Development of a Phase Assignment Tool Able to Distinguish between G2 and Mitotic Cells
by Steven Watson, Harry Porter, Ian Sudbery and Ruth Thompson
Int. J. Mol. Sci. 2024, 25(9), 4589; https://doi.org/10.3390/ijms25094589 - 23 Apr 2024
Viewed by 1299
Abstract
Single-cell RNA sequencing (scRNAseq) is a rapidly advancing field enabling the characterisation of heterogeneous gene expression profiles within a population. The cell cycle phase is a major contributor to gene expression variance between cells and computational analysis tools have been developed to assign [...] Read more.
Single-cell RNA sequencing (scRNAseq) is a rapidly advancing field enabling the characterisation of heterogeneous gene expression profiles within a population. The cell cycle phase is a major contributor to gene expression variance between cells and computational analysis tools have been developed to assign cell cycle phases to cells within scRNAseq datasets. Whilst these tools can be extremely useful, all have the drawback that they classify cells as only G1, S or G2/M. Existing discrete cell phase assignment tools are unable to differentiate between G2 and M and continuous-phase-assignment tools are unable to identify a region corresponding specifically to mitosis in a pseudo-timeline for continuous assignment along the cell cycle. In this study, bulk RNA sequencing was used to identify differentially expressed genes between mitotic and interphase cells isolated based on phospho-histone H3 expression using fluorescence-activated cell sorting. These gene lists were used to develop a methodology which can distinguish G2 and M phase cells in scRNAseq datasets. The phase assignment tools present in Seurat were modified to allow for cell cycle phase assignment of all stages of the cell cycle to identify a mitotic-specific cell population. Full article
(This article belongs to the Special Issue Latest Progress in DNA Damage and DNA Repair)
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19 pages, 3172 KiB  
Article
CSB Regulates Pathway Choice in Response to DNA Replication Stress Induced by Camptothecin
by Nicole L. Batenburg, John R. Walker and Xu-Dong Zhu
Int. J. Mol. Sci. 2023, 24(15), 12419; https://doi.org/10.3390/ijms241512419 - 4 Aug 2023
Cited by 1 | Viewed by 1973
Abstract
Topoisomerase inhibitor camptothecin (CPT) induces fork stalling and is highly toxic to proliferating cells. However, how cells respond to CPT-induced fork stalling has not been fully characterized. Here, we report that Cockayne syndrome group B (CSB) protein inhibits PRIMPOL-dependent fork repriming in response [...] Read more.
Topoisomerase inhibitor camptothecin (CPT) induces fork stalling and is highly toxic to proliferating cells. However, how cells respond to CPT-induced fork stalling has not been fully characterized. Here, we report that Cockayne syndrome group B (CSB) protein inhibits PRIMPOL-dependent fork repriming in response to a low dose of CPT. At a high concentration of CPT, CSB is required to promote the restart of DNA replication through MUS81–RAD52–POLD3-dependent break-induced replication (BIR). In the absence of CSB, resumption of DNA synthesis at a high concentration of CPT can occur through POLQ–LIG3-, LIG4-, or PRIMPOL-dependent pathways, which are inhibited, respectively, by RAD51, BRCA1, and BRCA2 proteins. POLQ and LIG3 are core components of alternative end joining (Alt-EJ), whereas LIG4 is a core component of nonhomologous end joining (NHEJ). These results suggest that CSB regulates fork restart pathway choice following high-dosage CPT-induced fork stalling, promoting BIR but inhibiting Alt-EJ, NHEJ, and fork repriming. We find that loss of CSB and BRCA2 is a toxic combination to genomic stability and cell survival at a high concentration of CPT, which is likely due to accumulation of ssDNA gaps, underscoring an important role of CSB in regulating the therapy response in cancers lacking functional BRCA2. Full article
(This article belongs to the Special Issue Latest Progress in DNA Damage and DNA Repair)
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