In the early embryonic period cells have a determined length of telomere endings.
As organism develops by cell differentiation, cells keep proliferating and during each division, telomeres get shorter because of replication mechanism specificity.
So nature determined that as organism get older, telomeres get shorter and cell goes to death.
When telomeres reach critical length there are several ways for cell to go further: apoptosis, malignancy, and necrosis.
By imposing a limit on the proliferative lifespan of most somatic cells, telomere erosion represents an innate mechanism for tumor suppression and may contribute to age-related disease.
A detailed understanding of the pathways that linked shortened telomeres to replicative senescence has been severely hindered by the inability of current methods to analyze telomere dynamics in detail.
Scientists described single telomere length analysis (STELA), a PCR-based approach where it was accurately measured the full spectrum of telomere lengths from individual chromosomes.
By STELA analysis of human XpYp telomeres in fibroblasts they identified several features of telomere biology.
Scientists have observed bimodal distributions of telomeres in normal fibroblasts; these distributions resulted from inter-allelic differences of up to 6.5 kb, this indicated that unexpectedly large-scale differences in zygotic telomere length were maintained throughout development.
Most telomeres shorten in a gradual fashion consistent with simple losses through end replication, and the rates of erosion are independent of allele size.
Superimposed on this are occasional, more substantial changes in length, which may be the consequence of additional mutational mechanisms.
Notably, some alleles showed almost complete loss of TTAGGG repeats at senescence.