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5.1
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Cells
Special Issues
Telomeres at the Crossroad of DNA Repair Pathways
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Telomeres at the Crossroad of DNA Repair Pathways

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Nuclei: Function, Transport and Receptors".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 6089

Special Issue Editor

Dr. Antonio Porro

E-Mail Website
Guest Editor
Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland
Interests: DNA damage response; DNA repair; telomere biology; replication; cell cycle

Special Issue Information

Dear Colleagues,

The fields of telomere biology and DNA repair have experienced convergence and cross-fertilization throughout years. Seminal contributions from both fields have been awarded Nobel prizes in Physiology-Medicine and Chemistry, in 2009 and 2015, respectively. In particular, the understanding of telomere biology provides but at the same time requires insights into the nature and regulation of DNA repair pathways. Telomeres function at chromosome ends to block unwarranted activation of DNA repair machineries. Therefore, knowledge of DNA damage response (DDR) pathways may unveil the regulatory nodes that lie at the interface between telomere biology and repair processes. DDR factors serve protective roles and help preserve telomere integrity. Conversely, dysfunctional telomeres have provided a platform for a better understanding of the nature of cellular DDR, unveiling specific aspects that are otherwise not readily evident from the analysis of genomic DNA damage. This Special Issue is therefore meant to focus on the convergence of DNA repair mechanisms and telomere biology and aims to foster a stimulating interdisciplinary synergy between these two fields.

Dr. Antonio Porro
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 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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • telomeres
  • DNA repair
  • DNA damage
  • response

Published Papers (2 papers)

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Research

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13 pages, 8519 KiB  
Article
Single Cell Analysis of Gastric Cancer Reveals Non-Defined Telomere Maintenance Mechanism
by Ji-Yong Sung and Jae-Ho Cheong
Cells 2022, 11(21), 3342; https://doi.org/10.3390/cells11213342 - 23 Oct 2022
Cited by 3 | Viewed by 2283
Abstract
Telomere maintenance mechanisms (TMMs) are important for cell survival and homeostasis. However, most related cancer research studies have used heterogenous bulk tumor tissue, which consists of various single cells, and the cell type properties cannot be precisely recognized. In particular, cells exhibiting non-defined [...] Read more.
Telomere maintenance mechanisms (TMMs) are important for cell survival and homeostasis. However, most related cancer research studies have used heterogenous bulk tumor tissue, which consists of various single cells, and the cell type properties cannot be precisely recognized. In particular, cells exhibiting non-defined TMM (NDTMM) indicate a poorer prognosis than those exhibiting alternative lengthening of telomere (ALT)-like mechanisms. In this study, we used bioinformatics to classify TMMs by cell type in gastric cancer (GC) in single cells and compared the biological processes of each TMM. We elucidated the pharmacological vulnerabilities of NDTMM type cells, which are associated with poor prognosis, based on molecular mechanisms. We analyzed differentially expressed genes in cells exhibiting different TMMs in two single-cell GC cohorts and the pathways enriched in single cells. NDTMM type cells showed high stemness, epithelial–mesenchymal transition, cancer hallmark activity, and metabolic reprogramming with mitochondrial abnormalities. Nuclear receptor subfamily 4 group A member 1 (NR4A1) activated parkin-dependent mitophagy in association with tumor necrosis factor-alpha (TNFA) to maintain cellular homeostasis without TMM. NR4A1 overexpression affected TNFA-induced GC cell apoptosis by inhibiting Jun N-terminal kinase/parkin-dependent mitophagy. Our findings also revealed that NR4A1 is involved in cell cycle mediation, inflammation, and apoptosis to maintain cell homeostasis, and is a novel potential therapeutic target in recalcitrant GC. Full article
(This article belongs to the Special Issue Telomeres at the Crossroad of DNA Repair Pathways)
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Review

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22 pages, 1977 KiB  
Review
To Fix or Not to Fix: Maintenance of Chromosome Ends Versus Repair of DNA Double-Strand Breaks
by Erika Casari, Marco Gnugnoli, Carlo Rinaldi, Paolo Pizzul, Chiara Vittoria Colombo, Diego Bonetti and Maria Pia Longhese
Cells 2022, 11(20), 3224; https://doi.org/10.3390/cells11203224 - 14 Oct 2022
Cited by 7 | Viewed by 3319
Abstract
Early work by Muller and McClintock discovered that the physical ends of linear chromosomes, named telomeres, possess an inherent ability to escape unwarranted fusions. Since then, extensive research has shown that this special feature relies on specialized proteins and structural properties that confer [...] Read more.
Early work by Muller and McClintock discovered that the physical ends of linear chromosomes, named telomeres, possess an inherent ability to escape unwarranted fusions. Since then, extensive research has shown that this special feature relies on specialized proteins and structural properties that confer identity to the chromosome ends, thus allowing cells to distinguish them from intrachromosomal DNA double-strand breaks. Due to the inability of conventional DNA replication to fully replicate the chromosome ends and the downregulation of telomerase in most somatic human tissues, telomeres shorten as cells divide and lose this protective capacity. Telomere attrition causes the activation of the DNA damage checkpoint that leads to a cell-cycle arrest and the entering of cells into a nondividing state, called replicative senescence, that acts as a barrier against tumorigenesis. However, downregulation of the checkpoint overcomes this barrier and leads to further genomic instability that, if coupled with re-stabilization of telomeres, can drive tumorigenesis. This review focuses on the key experiments that have been performed in the model organism Saccharomyces cerevisiae to uncover the mechanisms that protect the chromosome ends from eliciting a DNA damage response, the conservation of these pathways in mammals, as well as the consequences of their loss in human cancer. Full article
(This article belongs to the Special Issue Telomeres at the Crossroad of DNA Repair Pathways)
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