In short
A telomere is a repetitive DNA sequence capping the end of each chromosome that protects it from degradation, and that shortens slightly with every cell division.
DNA replication cannot fully copy the very end of a linear chromosome — a limitation called the end-replication problem. Telomeres, made of thousands of repeats of the sequence TTAGGG bound by protective proteins, act as a buffer that absorbs this loss without eroding genes that actually code for something. Each division shortens the telomere slightly, and once telomeres become critically short, the cell typically stops dividing and becomes senescent, or in some cases undergoes apoptosis.
Elizabeth Blackburn, Carol Greider, and Jack Szostak shared the 2009 Nobel Prize in Physiology or Medicine for discovering telomeres and telomerase, the enzyme that can rebuild telomere length. Most adult human somatic cells have very low telomerase activity, which is why telomeres shorten progressively over a lifetime; stem cells, germ cells, and (notably) most cancer cells maintain high telomerase activity, which is part of how cancer cells achieve unlimited replication.
Telomere length correlates with age at a population level and is associated with some age-related diseases in epidemiological studies, but consumer telomere-length tests are a poor predictor of an individual's biological age or disease risk — telomere length varies enormously between cells and tissues in the same person, and measurement methods (qPCR vs. Southern blot vs. flow-FISH) disagree with each other substantially. Epigenetic clocks have generally shown stronger correlation with age-related outcomes than telomere length in head-to-head comparisons.
Worth remembering
- Protective repetitive DNA cap that shortens with each cell division.
- Critically short telomeres trigger senescence or apoptosis.
- Individual telomere-length tests are noisy and a weak predictor compared with epigenetic clocks.