This review explores how telomere structure affects cell fate decisions, implicating mitotic processes and specific proteins.
Telomeres are nucleoprotein elements bound by shelterin that protect chromosome ends from DNA damage signalling and inappropriate repair. A defining architectural feature is the telomere loop (t-loop), a lariat structure formed by 3' overhang invasion into duplex telomeric DNA, which sequesters chromosome ends from damage recognition. T-loop stability is disrupted by the loss of the shelterin component TRF2, and progressive telomere shortening during ageing is predicted to compromise t-loop maintenance. In addition to intrinsic erosion, an active, shelterin-directed mechanism unwinds t-loops during mitotic arrest. This mitotic arrest-dependent telomere deprotection promotes mitotic death, requires Aurora B kinase-dependent shelterin phosphorylation and the BTR complex, and is opposed by WRN. In this review, we review how dynamic t-loop architecture integrates telomere signalling with cell fate decisions.
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Hayashi et al. (2026) studied this question.
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