DNA excision repair at telomeres |
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| Institution: | 1. Elson S. Floyd College of Medicine, United States;2. School of Molecular Biosciences, Washington State University, United States;1. Department of Cell Biology, Skirball Institute of Biomolecular Medicine, NYU School of Medicine, New York, NY 10016, USA;2. Department of Chemistry and Biochemistry, University of Colorado, Boulder, CO 80309, USA;3. Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA;4. Department of Biochemistry and Molecular Pharmacology, NYU School of Medicine, New York, NY 10016, USA;5. Departments of Dermatology and Biochemistry and Molecular Genetics, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA;1. University of Vienna, Research Platform Active Ageing, Althanstraße 14, 1090 Vienna, Austria;2. Queensland University of Technology, Faculty of Health, School of Biomedical Sciences, Institute of Health and Biomedical Innovation (IHBI), Tissue Repair and Regeneration Group, 60 Musk Avenue, Kelvin Grove Campus, Brisbane, QLD 4059, Australia;3. University of Vienna, Faculty of Life Sciences, Department of Nutritional Sciences, Althanstraße 14, 1090 Vienna, Austria;1. Clare Hall Laboratories, London Research Institute, Cancer Research UK, Clare Hall, South Mimms, Hertfordshire EN6 3LD, UK;2. Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA;1. Developmental and Stem Cell Biology Division, Victor Chang Cardiac Research Institute, Darlinghurst NSW, Australia;2. St. Vincent''s Clinical School, University of New South Wales, Kensington NSW, Australia;1. Regeneration and Aging Group, Centro Nacional de Investigaciones Cardiovasculares (CNIC-ISCIII), Melchor Fernández Almagro 3, 28029 Madrid, Spain;2. Development of the Epicardium and Its Role during Regeneration Group, Centro Nacional de Investigaciones Cardiovasculares (CNIC-ISCIII), Melchor Fernández Almagro 3, 28029 Madrid, Spain;3. Cardiovascular Imaging in Humans, Centro Nacional de Investigaciones Cardiovasculares (CNIC-ISCIII), Melchor Fernández Almagro 3, 28029 Madrid, Spain;4. Bioinformatic Unit, Centro Nacional de Investigaciones Cardiovasculares (CNIC-ISCIII), Melchor Fernández Almagro 3, 28029 Madrid, Spain;5. Electron Microscopy Center, Complutense University, Madrid 28040, Spain |
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| Abstract: | DNA damage is caused by either endogenous cellular metabolic processes such as hydrolysis, oxidation, alkylation, and DNA base mismatches, or exogenous sources including ultraviolet (UV) light, ionizing radiation, and chemical agents. Damaged DNA that is not properly repaired can lead to genomic instability, driving tumorigenesis. To protect genomic stability, mammalian cells have evolved highly conserved DNA repair mechanisms to remove and repair DNA lesions. Telomeres are composed of long tandem TTAGGG repeats located at the ends of chromosomes. Maintenance of functional telomeres is critical for preventing genome instability. The telomeric sequence possesses unique features that predispose telomeres to a variety of DNA damage induced by environmental genotoxins. This review briefly describes the relevance of excision repair pathways in telomere maintenance, with the focus on base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR). By summarizing current knowledge on excision repair of telomere damage and outlining many unanswered questions, it is our hope to stimulate further interest in a better understanding of excision repair processes at telomeres and in how these processes contribute to telomere maintenance. |
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| Keywords: | Telomere Base excision repair Nucleotide excision repair Mismatch repair Genome stability |
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