Pot1 and cell cycle progression cooperate in telomere length regulation
Open accessAbstract
Removal of the vertebrate telomere protein Pot1 results in a DNA damage response and cell cycle arrest. Here we show that loss of chicken Pot1 causes Chk1 activation, and inhibition of Chk1 signaling prevents the cell cycle arrest. However, arrest still occurs after disruption of ATM, which encodes another DNA damage response protein. These results indicate that Pot1 is required to prevent a telomere checkpoint mediated by another such protein, ATR, that is most likely triggered by the G-overhang. We also show that removal of Pot1 causes exceptionally rapid telomere growth upon arrest in late S/G2 of the cell cycle. However, release of the arrest slows both telomere growth and G-overhang elongation. Thus, Pot1 seems to regulate telomere length and G-overhang processing both through direct interaction with the telomere and by preventing a late S/G2 delay in the cell cycle. Our results reveal that cell cycle progression is an important component of telomere length regulation.
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Dysfunctional telomeres activate upstream checkpoint PI3 kinases such as ATM or ATR.
“Dysfunctional telomeres activate upstream checkpoint PI3 kinases, such as ATM (ataxia-telangiectasia mutated) or ATR (ataxia-telangiectasia and Rad3 related)22, 27-30”
From Telomere dysfunction and tumour suppression: the senescence connection (2008) · cites this paper as [28]
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- Authors
- Churikov, D., & Price, C. M.
- Affiliations
- University of Cincinnati (US)
- Corresponding author
- Price, Carolyn M
- Venue
- Nature Structural & Molecular Biology
- Published
- 2007-12-09
- Volume
- 15
- Issue
- 1
- Pages
- 79-84
- ISSN
- 1545-9985 (ISSN-L)
- 1545-9993
- PMC
- PMC2516480
- OpenAlex
- W2055185717
- Cited by
- 67
- References
- 50
- Citations by year
- 2026: 1 · 2024: 2 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 3 · 2019: 2 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 2 · 2014: 6 · 2013: 2 · 2012: 7
- FWCI
- 6.01
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Structural & Molecular Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences (GM 041803, R01GM041803)
- 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
- POT1, telomere length regulation, cell cycle arrest, ATM, ATR, DNA damage response, chickens
- MeSH terms
- Wortmannin, Shelterin Complex, Androstadienes, Caffeine, Carbazoles, Cell Cycle, Cell Line, DNA-Binding Proteins, Enzyme Inhibitors, Flow Cytometry, Humans, Indoles, Kinetics, Tamoxifen, G2 Phase, S Phase, Telomere, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Tumor Suppressor Proteins, Telomere-Binding Proteins, Ataxia Telangiectasia Mutated Proteins
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