Biometris, Wageningen University and Research Centre, P.O. Box 100, 6700AC Wageningen, The Netherlands.
J Theor Biol. 2011 Aug 7;282(1):1-6. doi: 10.1016/j.jtbi.2011.04.026. Epub 2011 May 11.
It was recently shown that, within individuals, longer telomeres shorten at a higher rate. This explorative study deals with a mathematical model of this process. It is a nonlinear differential equation describing length-dependent decrease that can be linked to a Poisson process. The model also takes in account telomere shortening due to the end replication problem. Parameters are fitted using data from samples of red blood cells of free-living juvenile corvids. The Poisson process can be related to oxidative stress causing DNA strand breaks. The shortest telomeres in a genome are the best predictors of survival, and one can therefore hypothesize on functional grounds that short telomeres should be better protected by some control mechanism in the cellular system. However, the present study shows that such a mechanism is not required to explain length-dependent telomere shortening: agents of telomere shortening such as oxidative stress with a certain strength modeled by a Poisson process with an appropriately chosen parameter suffice to generate the observed pattern.
最近的研究表明，在个体内部，较长的端粒会以更高的速度缩短。本探索性研究涉及到对这一过程的数学模型的研究。这是一个描述长度依赖性衰减的非线性微分方程，可以与泊松过程相关联。该模型还考虑了由于端复制问题导致的端粒缩短。参数是使用来自自由生活的幼年雀形目鸟类的红细胞样本中的数据进行拟合的。泊松过程可以与导致 DNA 链断裂的氧化应激相关联。基因组中最短的端粒是生存的最佳预测因子，因此，可以从功能角度假设，细胞系统中的某些控制机制应该更好地保护短端粒。然而，本研究表明，这种机制并不需要解释长度依赖性的端粒缩短：通过泊松过程模拟具有一定强度的氧化应激等端粒缩短剂，并用适当选择的参数，就足以产生观察到的模式。
