DNA damage response at functional and dysfunctional telomeres
Open Access
- 15 January 2008
- journal article
- review article
- Published by Cold Spring Harbor Laboratory in Genes & Development
- Vol. 22 (2) , 125-140
- https://doi.org/10.1101/gad.1626908
Abstract
The ends of eukaryotic chromosomes have long been defined as structures that must avoid being detected as DNA breaks. They are protected from checkpoints, homologous recombination, end-to-end fusions, or other events that normally promote repair of intrachromosomal DNA breaks. This differentiation is thought to be the consequence of a unique organization of chromosomal ends into specialized nucleoprotein complexes called telomeres. However, it is becoming increasingly clear that proteins governing the DNA damage response are intimately involved in the regulation of telomeres, which undergo processing and structural changes that elicit a transient DNA damage response. This suggests that functional telomeres can be recognized as DNA breaks during a temporally limited window, indicating that the difference between a break and a telomere is less defined than previously assumed.Keywords
This publication has 183 references indexed in Scilit:
- Telomere lengthening early in developmentNature Cell Biology, 2007
- Mrc1 protects uncapped budding yeast telomeres from exonuclease EXO1DNA Repair, 2007
- Telomerase and Tel1p Preferentially Associate with Short Telomeres in S. cerevisiaeMolecular Cell, 2007
- Dual role for Saccharomyces cerevisiae Tel1 in the checkpoint response to double‐strand breaksEMBO Reports, 2007
- The Checkpoint Clamp Activates Mec1 Kinase during Initiation of the DNA Damage CheckpointMolecular Cell, 2006
- POT1b protects telomeres from end-to-end chromosomal fusions and aberrant homologous recombinationThe EMBO Journal, 2006
- The Telomeric Protein TRF2 Binds the ATM Kinase and Can Inhibit the ATM-Dependent DNA Damage ResponsePLoS Biology, 2004
- Anatomy and Dynamics of DNA Replication Fork Movement in Yeast Telomeric RegionsMolecular and Cellular Biology, 2004
- DNA Damage Foci at Dysfunctional TelomeresCurrent Biology, 2003
- DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociationNature, 2003