2006/09/30 by Tibor Antal, T. Antal, Krastan B. Blagoev +3 · 1 citation
Biochemistry, Genetics and Molecular Biology · Medicine · Physics and Astronomy · #Genetics, Aging, and Longevity in Model Organisms #Telomeres, Telomerase, and Senescence #cond-mat.stat-mech #physics.bio-ph #q-bio.CB
paper · pdf · doi:10.1016/j.jtbi.2007.06.009
published as Journal of Theoretical Biology 248, 411-417 (2007) · 6 pages, 1 figure, 2-column revtex4 format; version 2: final published form; contains various improvements in response to referee comments
openalex publication_date 2007/06/14 · arxiv created 2008/04/23 · arxiv updated 2009/12/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01
We investigate a model of cell division in which the length of telomeres within the cell regulate their proliferative potential. At each cell division the ends of linear chromosomes change and a cell becomes senescent when one or more of its telomeres become shorter than a critical length. In addition to this systematic shortening, exchange of telomere DNA between the two daughter cells can occur at each cell division. We map this telomere dynamics onto a biased branching diffusion process with an absorbing boundary condition whenever any telomere reaches the critical length. As the relative effects of telomere shortening and cell division are varied, there is a phase transition between finite lifetime and infinite proliferation of the cell population. Using simple first-passage ideas, we quantify the nature of this transition.