Recent hypothesis connects the origin of aging with telomere loss due to "end-replication problem" of linear chromosomes. It is interesting that in some cases the mutant cells which lost all telomeric DNA sequences became immortal, because all chromosomes in these cells became circular. The mechanism of chromosome circularization is not yet known since despite progress in understanding the structure and function of individual genes, little is known about the chromatin structure beyond the level of the nucleosome. Some authors proposed that the base of linear eukaryotic chromosome should be the giant DNA ring. From this standpoint it is clear that if the telomeres facilitate a rod-like shape to originally circular chromosome, the telomere absence simply reveals intrinsic design of hereditary matter with no ends. In favor of this view, a lot of telomeric DNA sequences are presented at non-telomeric sites of vertebrate chromosomes. The origin and purpose of such an intrachromosomal location of telomeric sequences are unknown. Perhaps, they are important for additional anchoring of the chromosome to the inner nuclear membrane and matrix and/or for facilitation of a chromosome rod-like design development. However, more data are needed to prove/disprove this "circular whole chromosome DNA hypothesis". In effect, there are the real mechanisms for telomere maintenance in all kinds of somatic stem cells. Moreover, age does not significantly alter the capacity for telomerase induction in such kind of somatic cells as human lymphocytes. Hence, the pure telomere shortening hypothesis of aging meets some difficulties and has to be modified.
Telomere-related aging hypothesis
Intrachromosomal telomeric sequences