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Updated: Aug 19, 2026

Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Is 'senescence' of diploid cells an ad hoc mechanism suppressing 'replicon' or not?
1Department of Orthopedic Surgery, Gunma University School of Medicine, Japan.
Abstract:
So-called 'limited life span' of diploid cells does not depend on their unresponsiveness to growth factors from the data obtained by complete protein-free culture of tumor cells. Limited proliferation (called limited life span) of diploid cells is one of the 'ad-hoc' negative regulatory mechanisms in animals, and can not be differentiated from other inhibitory mechanisms called 'tumor suppression' and 'terminal differentiation'. Metabolic imbalance induced by proliferation-dependent time-bomb mechanisms including infidelity of DNA repair is suggested to explain limited proliferation of cells. After maturation, autonomic progression of negative regulators in cells is induced by no prohibition of terminal differentiation, since organisms prepare no programs to stop development and differentiation. It is an attractive hypothesis that a proliferation-dependent time-bomb has been developed to control organogenesis for maturation and to determine body size. It is true that limited proliferation of cells can not explain longevity of individuals, although the so-called longevity genes play roles in ageing. Teleologically, longevity of individuals has been developed to produce genetic heterogeneity according to the selfish gene theory. This inter- and intra-species genetic heterogeneity increases the probability of selfish gene replication in germ cell line. After maturation and reproduction of DNA in germ cell line, individuals as vehicles for the DNA can be discarded by the 'selfish' genes.
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