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J Theor Biol. 1999 May 21;198(2):259-68.

Intramitotic and intraclonal variation in proliferative potential of human diploid cells: explained by telomere shortening.

Author information

1
Department of Biochemistry and Biophysics, Center for Developmental Biology, College of Life Sciences, Wuhan University, Wuhan 430072, People's Republic of China. tanclswu@public.wh.hb.cn

Abstract

Normal human diploid cells can only divide for a limited number of times (known as the Hayflick limit). They manifest two unique features during in vitro senescence. The division capability of individual cells in a clone, though all derived from a same ancestor, is heterogeneous with a distinct bimodal distribution. Two sister cells derived from a same parent cell can have a large difference in their doubling potentials. These two unique features have not been properly explained by any known physiological process since their observation in 1980. Here I represent a telomere-shortening model based on recent experimental measurement of telomere deletion in human cells. Using computer simulation, I show that the model satisfactorily explains the intraclonal and intramitotic variation in division capability of human diploid cells. Moreover, the simulations predict that human cells may only monitor the shortening of a few, most likely two, telomeres to regulate their proliferative potential.

PMID:
10339397
DOI:
10.1006/jtbi.1999.0914
[Indexed for MEDLINE]

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