Abstract
How a cell distinguishes a double-strand break from the end of a chromosome has long fascinated cell biologists. It was thought that the protection of chromosomal ends required either a telomere-specific complex or the looping back of the 3' TG-rich overhang to anneal with a homologous double-stranded repeat. These models must now accommodate the findings that complexes involved in nonhomologous end joining play important roles in normal telomere length maintenance, and that subtelomeric chromatin changes in response to the DNA damage checkpoint. A hypothetical chromatin assembly checkpoint may help to explain why telomeres and the double-strand break repair machinery share essential components.
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