Telomeres protect ends of chromosomes from fraying and undesired DNA repair. TRF2, a component of the telomere-specific shelterin protein complex, facilitates end protection and prevents chromosome fusions via sequestration of the terminal telomere repeat sequence within a T-loop structure; deleting TRF2 in somatic cells abolishes T-loop formation, resulting in chromosome end-to-end fusions and cell death. Surprisingly, two papers in Nature—by Simon Boulton and colleagues, and Eros Lazzerini Denchi and colleagues—now show that TRF2 is largely dispensable for chromosome end protection in pluripotent embryonic and epiblast stem cells: in these cells, telomere protection is provided in a different manner as T-loops form independently of TRF2.
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