How Telomeres Solve the End-Protection Problem
By T. de Lange. Science, 2009
836 citations recorded by the source corpus.
The ends of eukaryotic chromosomes have the potential to be mistaken for damaged or broken DNA and must therefore be protected from cellular DNA damage response pathways. Otherwise, cells might permanently arrest in the cell cycle, and attempts to “repair” the chromosome ends would have devastating consequences for genome integrity. This end-protection problem is solved by protein-DNA complexes called telomeres. Studies of mammalian cells have recently uncovered the mechanism by which telomeres disguise the chromosome ends. Comparison to unicellular eukaryotes reveals key differences in the DNA damage response systems that inadvertently threaten chromosome ends. Telomeres appear to be tailored to these variations, explaining their variable structure and composition.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/dd07f653387a1c3cbe10537913e5935eac4374ba
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
In Physiology
Citations in the corpus
- Increased brood size leads to persistent eroded telomeres (2014, positive): “Oxidative stress accelerates telomere loss (Von Zglinicki, 2002; Haussmann et al., 2011; Blackburn and Epel, 2012) while telomerase activity (mainly active in germinal and stem cells) and shelterin protein complex stability favor telomere maintenance (Blackburn, 2000; De Lange, 2009).”
- How shelterin solves the telomere end-protection problem. (2010, background): “The rampant NHEJ at telomeres typical of TRF2-deficient cells is largely abrogated when the ATM kinase is not present (Lazzerini Denchi and de Lange 2007; Dimitrova and de Lange 2009).”
- Telomere dysfunction in ageing and age-related diseases (2022, methodology): “These include the following techniques: (1) Southern blotting, which measures mean telomere length using the length distribution of the terminal restriction fragments; (2) quantitative PCR (qPCR), which measures the ratio of telomere repeat copy number to single copy gene copy number; (3) single tel”