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Mathematical modeling of cell cycle regulation in response to DNA damage: Exploring mechanisms of cell-fate determination by Kazunari Iwamoto; Hiroyuki Hamada; Yukihiro Eguchi; Masahiro Okamoto is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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After DNA damage, cells activate p53, a tumor suppressor gene, and select a cell fate (e.g., DNA repair, cell cycle arrest, or apoptosis). Recently, a p53 oscillatory behavior was observed following DNA damage. However, the relationship between this p53 oscillation and cell-fate selection is unclear. Here, we present a novel model of the DNA damage signaling pathway that includes p53 and whole cell cycle regulation and explore the relationship between p53 oscillation and cell fate selection. The simulation run without DNA damage qualitatively realized experimentally observed data from several cell cycle regulators, indicating that our model was biologically appropriate. Moreover, the comprehensive sensitivity analysis for the proposed model was implemented by changing the values of all kinetic parameters, which revealed that the cell cycle regulation system based on the proposed model has robustness on a fluctuation of reaction rate in each process. Simulations run with four different intensities of DNA damage, i.e. Low-damage, Medium-damage, High-damage, and Excess-damage, realized cell cycle arrest in all cases. Low-damage, Medium-damage, High-damage, and Excess-damage correspond

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Author

Kazunari Iwamoto; Hiroyuki Hamada; Yukihiro Eguchi; Masahiro Okamoto

Publisher

Elsevier Science; Elsevier ; Elsevier BV (ISSN 0303-2647)

Published

2011

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)