Human RAP1 inhibits non‐homologous end joining at telomeres
Open accessAbstract
Telomeres, the nucleoprotein structures at the ends of linear chromosomes, promote genome stability by distinguishing chromosome termini from DNA double-strand breaks (DSBs). Cells possess two principal pathways for DSB repair: homologous recombination and non-homologous end joining (NHEJ). Several studies have implicated TRF2 in the protection of telomeres from NHEJ, but the underlying mechanism remains poorly understood. Here, we show that TRF2 inhibits NHEJ, in part, by recruiting human RAP1 to telomeres. Heterologous targeting of hRAP1 to telomeric DNA was sufficient to bypass the need for TRF2 in protecting telomeric DNA from NHEJ in vitro. On expanding these studies in cells, we find that recruitment of hRAP1 to telomeres prevents chromosome fusions caused by the loss of TRF2/hRAP1 from chromosome ends despite activation of a DNA damage response. These results provide the first evidence that hRAP1 inhibits NHEJ at mammalian telomeres and identify hRAP1 as a mediator of genome stability.
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Mammalian TRF2-interacting protein is recruited to telomeres through TRF2 and may help repress non-homologous end joining.
“Unlike yeast Rap1p, mammalian telomeric repeat binding factor 2-interacting protein does not bind telomeric DNA directly but is instead recruited to telomeres through its interaction with TRF2, where it may act to aid in repression of non-homologous end joining (11,12).”
From Telomeres and telomerase in cancer (2010) · cites this paper as [12]
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References 50 · Cited by 151
Research works printed but not linked: 1
- Poon SS, Lansdorp PM (2001) Quantitative fluorescence in situ hybridization (Q-FISH). Curr Protoc Cell Biol, Chapter 18, Unit 1814
- Authors
- Sarthy, J., Bae, N. S., Scrafford, J., & Baumann, P.
- Affiliations
- Stowers Institute for Medical Research (US)
- Corresponding author
- Baumann, Peter
- Venue
- The EMBO Journal
- Published
- 2009-09-17
- Volume
- 28
- Issue
- 21
- Pages
- 3390-3399
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC2776107
- OpenAlex
- W2155514571
- Cited by
- 151
- References
- 50
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 10 · 2023: 6 · 2022: 5 · 2021: 14 · 2020: 5 · 2019: 6 · 2018: 10 · 2017: 8 · 2016: 10 · 2015: 8 · 2014: 10 · 2013: 8 · 2012: 13
- FWCI
- 9.72
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- The EMBO Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Pew Charitable Trusts
- Directorate for Biological Sciences
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- 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
- Keywords
- Rap1, TRF2, non-homologous end joining, telomeres, telomere protection, DNA double-strand break repair, chromosome fusion, genome stability, DNA damage response, telomeric DNA
- MeSH terms
- Shelterin Complex, DNA, DNA Damage, DNA Repair, DNA-Binding Proteins, HeLa Cells, Humans, Schizosaccharomyces, Gene Expression, Telomere, Schizosaccharomyces pombe Proteins, Telomere-Binding Proteins, Telomeric Repeat Binding Protein 2, Genomic Instability
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