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In Science this week, researchers at the Rockefeller University report on the role of Rap1, a conserved subunit of shelterin, which is an essential telomeric protein complex that prevents damage to DNA. In removing Rap1 from mouse telomeres via gene deletions or by replacing TRF2 with a mutant that doesn't bind Rap1, the team found that it is critical for the repression of homology-directed repair, which can alter telomere length.

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