POT1 recruits and regulates the CST-Polα/primase complex at human telomeres, ensuring proper telomere replication and maintenance. This process is vital for maintaining genome stability, which plays a key role in aging, longevity, and preventing age-related diseases linked to telomere dysfunction.
July 2024 – Cell
Key takeaways
- POT1 recruits CST-Polα/primase to maintain telomere integrity: POT1 is a protective protein that binds to the ends of telomeres. It ensures that the CST-Polα/primase complex, which is responsible for synthesizing new DNA strands, is properly recruited. This process is vital for ensuring that telomeres are accurately replicated during cell division, preventing them from becoming too short or unstable
- Proper telomere replication is crucial for genome stability: Telomeres act as protective caps on the ends of chromosomes, preventing them from degrading or fusing with other chromosomes. Efficient telomere replication ensures that cells maintain their genetic information over time. Genome stability helps prevent mutations and other damage that can contribute to cellular aging and dysfunction
- Telomere dysfunction accelerates aging and disease: When telomeres become critically short or are not properly maintained, they can no longer protect chromosomes. This leads to genomic instability, which is associated with various age-related diseases like cardiovascular disease, neurodegenerative disorders, and cancer. Telomere dysfunction is considered a hallmark of aging, contributing to the decline in tissue and organ function over time
By improving or preserving the function of telomere maintenance pathways—such as ensuring optimal activity of proteins like POT1—cells can potentially delay aging processes. Supporting these pathways may reduce the risk of age-related diseases and contribute to a longer healthspan, the period of life spent in good health.
Read the article at: Oganesyan, Vladislav, et al. “How POT1 Recruits and Regulates CST-Polα/Primase at Human Telomeres.” Cell, vol. 188, no. 18, 2024, pp. 3772-3786.