Aging and immortality in a cell proliferation model

被引:18
作者
Antal, T.
Blagoev, K. B.
Trugman, S. A.
Redner, S.
机构
[1] Boston Univ, Dept Phys, Ctr Polymer Studies, Boston, MA 02215 USA
[2] Harvard Univ, Program Evolutionary Dynam, Cambridge, MA 02138 USA
[3] Los Alamos Natl Lab, Div Theory, Los Alamos, NM 87545 USA
关键词
cell division; telomere dynamics; senescence;
D O I
10.1016/j.jtbi.2007.06.009
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
We investigate a model of cell division in which the length of telomeres within a cell regulates its proliferative potential. At each division, telomeres undergo a systematic length decrease as well as a superimposed fluctuation due to exchange of telomere DNA between the two daughter cells. A cell becomes senescent when one or more of its telomeres become shorter than a critical length. We map this telomere dynamics onto a biased branching-diffusion process with an absorbing boundary condition whenever any telomere reaches the critical length. Using first-passage ideas, we find a phase transition between finite lifetime and immortality (infinite proliferation) of the cell population as a function of the influence of telomere shortening, fluctuations, and cell division. (C) 2007 Elsevier Ltd. All rights reserved.
引用
收藏
页码:411 / 417
页数:7
相关论文
共 29 条
[1]  
Abramowitz M., 1970, HDB MATH FUNCTIONS
[2]   Frequent recombination in telomeric DNA may extend the proliferative life of telomerase-negative cells [J].
Bailey, SM ;
Brenneman, MA ;
Goodwin, EH .
NUCLEIC ACIDS RESEARCH, 2004, 32 (12) :3743-3751
[3]   Strand-specific postreplicative processing of mammalian telomeres [J].
Bailey, SM ;
Cornforth, MN ;
Kurimasa, A ;
Chen, DJ ;
Goodwin, EH .
SCIENCE, 2001, 293 (5539) :2462-2465
[4]  
BLAGOEV KB, 2005, P TELOMERES TELOMERA
[5]   Evidence for an alternative mechanism for maintaining telomere length in human tumors and tumor-derived cell lines [J].
Bryan, TM ;
Englezou, A ;
DallaPozza, L ;
Dunham, MA ;
Reddel, RR .
NATURE MEDICINE, 1997, 3 (11) :1271-1274
[6]   The biology of replicative senescence [J].
Campisi, J .
EUROPEAN JOURNAL OF CANCER, 1997, 33 (05) :703-709
[7]  
Campisi J, 2001, TRENDS CELL BIOL, V11, pS27, DOI 10.1016/S0962-8924(01)82148-6
[8]   Replicative senescence: An old lives' tale? [J].
Campisi, J .
CELL, 1996, 84 (04) :497-500
[9]  
CAREY JR, 1992, SCIENCE, V258, P457, DOI 10.1126/science.1411540
[10]   Damage segregation at fissioning may increase growth rates: A superprocess model [J].
Evans, Steven N. ;
Steinsaltz, David .
THEORETICAL POPULATION BIOLOGY, 2007, 71 (04) :473-490