Because eukaryotic chromosomes are linear and the replication machinery cannot copy a strand fully to its terminus, each round of DNA replication shortens the telomeres — non-coding protective caps at chromosome ends — so that a somatic mitotic cell can complete only a finite number of divisions, the Hayflick limit, before telomere attrition triggers a DNA damage response and the cell permanently withdraws from the cell cycle into replicative senescence. Senescence is a stable altered cell state, not cell death: the cell persists in the tissue, alters its gene expression, morphology, and interactions with neighbors, but cannot divide; its general function is to forestall propagation of DNA damage to daughter cells, and it can also be induced independently of telomere length by dysfunctional telomeres, mutation, or toxin-mediated DNA damage — the latter route being the only one available to post-mitotic cells, which cannot undergo replicative senescence because they do not replicate. The enzyme telomerase restores the telomeric sequence lost at each replication, sustaining unlimited division capacity in stem cells and, when aberrantly expressed in a somatic cell, permitting escape from senescence — one route to unchecked proliferation and tumor formation. This concept belongs to cell biology, at the interface of genome maintenance, aging, and cancer biology.
Because eukaryotic chromosomes are linear and the replication machinery cannot copy a strand fully to its terminus, each round of DNA replication shortens the telomeres — non-coding protective caps a…