RTEL1 Maintains Genomic Stability by Suppressing Homologous Recombination
Open accessAbstract
Homologous recombination (HR) is an important conserved process for DNA repair and ensures maintenance of genome integrity. Inappropriate HR causes gross chromosomal rearrangements and tumorigenesis in mammals. In yeast, the Srs2 helicase eliminates inappropriate recombination events, but the functional equivalent of Srs2 in higher eukaryotes has been elusive. Here, we identify C. elegans RTEL-1 as a functional analog of Srs2 and describe its vertebrate counterpart, RTEL1, which is required for genome stability and tumor avoidance. We find that rtel-1 mutant worms and RTEL1-depleted human cells share characteristic phenotypes with yeast srs2 mutants: lethality upon deletion of the sgs1/BLM homolog, hyperrecombination, and DNA damage sensitivity. In vitro, purified human RTEL1 antagonizes HR by promoting the disassembly of D loop recombination intermediates in a reaction dependent upon ATP hydrolysis. We propose that loss of HR control after deregulation of RTEL1 may be a critical event that drives genome instability and cancer.
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Five of the seven identified LTL-associated loci contain genes (TERC, TERT, NAF1, OBFC1, RTEL1) known to be involved in telomere biology.
“Five of the loci contain genes (TERC, TERT, NAF1, OBFC1, RTEL1) that are known to be involved in telomere biology.”
From Identification of seven loci affecting mean telomere length and their association with disease (2013) · cites this paper as [23]
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- Authors
- Barber, L. J., Youds, J. L., Ward, J. D., McIlwraith, M. J., O'Neil, N. J., Petalcorin, M. I. R., Martin, J. S., Collis, S. J., Cantor, S. B., Auclair, M., Tissenbaum, H., West, S. C., Rose, A. M., & Boulton, S. J.
- Affiliations
- Cancer Research UK (GB)
- University of British Columbia (CA)
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Boulton, Simon J.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2008-10
- Volume
- 135
- Issue
- 2
- Pages
- 261-271
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3726190
- OpenAlex
- W2032640722
- Cited by
- 369
- References
- 68
- Citations by year
- 2026: 7 · 2025: 15 · 2024: 14 · 2023: 19 · 2022: 16 · 2021: 16 · 2020: 20 · 2019: 19 · 2018: 20 · 2017: 18 · 2016: 25 · 2015: 24 · 2014: 24 · 2013: 26 · 2012: 33
- FWCI
- 10.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1750 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- Funders
- Cancer Research UK
- National Institute on Aging (R01AG031237, R01AG025891)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Keywords
- RTEL1, Srs2 helicase, homologous recombination, genome stability, DNA repair, hyper-recombination, DNA damage sensitivity, tumor suppression, ATP hydrolysis, Caenorhabditis elegans, DNA helicase
- MeSH terms
- Animals, DNA, DNA Repair, DNA Helicases, Humans, Mutation, Recombination, Genetic, Saccharomyces cerevisiae, Caenorhabditis elegans, Saccharomyces cerevisiae Proteins, Caenorhabditis elegans Proteins, Genomic Instability
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