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Linear chromosomes confer both benefits (1) and burdens on eukaryotic cells [HN1]. This new genome design has created two additional problems stemming from the fact that linear chromosomes have ends. Eukaryotes have had to evolve a strategy for the replication of terminal DNA, a task mostly executed by the enzyme telomerase [HN2] (2). Furthermore, chromosome termini must be “capped,” otherwise they will be identified as damaged DNA and subjected to DNA repair [HN3], an outcome that would cause loss of chromosome integrity and cell viability. In essence, the capping problem has been solved by the presence of telomeres [HN4], complexes of DNA and protein that protect the ends of chromosomes. However, the ways in which various organisms protect their telomeres appear to be remarkably idiosyncratic. Ciliates [HN5], budding yeast [HN6], and mammals each seem to have arrived at a different system (see the figure), providing a perplexing diversity of mechanisms to solve such a fundamental problem. Data presented by Baumann and Cech [HN7] on page 1171 of this issue suggest that, in all cases, telomeres are protected by a capping protein that binds to the single-stranded DNA commonly found at the ends of chromosomes (3).
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