They are essential for normal chromosome replication, and since their length shortens a bit with each replication, they are believed to be involved in the aging of the cell. The obvious significance of senescence to organismal aging and the development of cancer has engendered a long-lasting and lively debate about its mechanisms. Two major theories have been used to explain limited replicative capacity. The second theory is now believed to be generally true. It is known that cell senescence can be overcome, because many cell lines in common laboratory use are quite obviously immortal.
Rodent cells can overcome senescence spontaneously.
Human, chicken, bovine, and horse cells rarely, if ever, immortalize spontaneously. Certain viral or biochemical interventions in human cell cultures can overcome cell senescence, typically by causing 20 to 30 extra population doublings. The current prevailing hypothesis for the nature of the molecular clock involved in cell senescence is the attrition of telomeres. The author proposes that immortalization of human cells requires a bypass of both cell senescence and crisis, whereas in rodent cells cell crisis does not exist and culture lifespan is limited only by senescence. The author suggests that although it remains to be rigorously demonstrated, this strongly implies that activation of telomerase can result in one-step immortalization.