Leinheiser Anna K, Mitchell Colleen C, Rooke Ethan, Strack Stefan, Grueter Chad E
Department of Mathematics, University of Iowa, Iowa City, Iowa, United States of America.
Department of Internal Medicine, Division of Cardiovascular Medicine, Francois M. Abboud Cardiovascular Research Center, Fraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, Iowa, United States of America.
PLoS Comput Biol. 2024 Nov 18;20(11):e1012596. doi: 10.1371/journal.pcbi.1012596. eCollection 2024 Nov.
Mitochondrial hyperfission in response to cellular insult is associated with reduced energy production and programmed cell death. Thus, there is a critical need to understand the molecular mechanisms coordinating and regulating the complex process of mitochondrial fission. We develop a nonlinear dynamical systems model of dynamin related protein one (Drp1)-dependent mitochondrial fission and use it to identify parameters which can regulate the total fission rate (TFR) as a function of time. The TFR defined from a nondimensionalization of the model undergoes a Hopf bifurcation with bifurcation parameter [Formula: see text] where [Formula: see text] is the total concentration of mitochondrial fission factor (Mff) and k+ and k- are the association and dissociation rate constants between oligomers on the outer mitochondrial membrane. The variable μ can be thought of as the maximum build rate over the disassembling rate of oligomers. Though the nondimensionalization of the system results in four dimensionless parameters, we found the TFR and the cumulative total fission (TF) depend strongly on only one, μ. Interestingly, the cumulative TF does not monotonically increase as μ increases. Instead it increases with μ to a certain point and then begins to decrease as μ continues to increase. This non-monotone dependence on μ suggests interventions targeting k+, k-, or [Formula: see text] may have a non-intuitive impact on the fission mechanism. Thus understanding the impact of regulatory parameters, such as μ, may assist future therapeutic target selection.
细胞受到损伤时线粒体的过度分裂与能量产生减少和程序性细胞死亡相关。因此,迫切需要了解协调和调节线粒体分裂这一复杂过程的分子机制。我们建立了一种依赖发动蛋白相关蛋白1(Drp1)的线粒体分裂的非线性动力学系统模型,并使用该模型来确定作为时间函数调节总分裂率(TFR)的参数。从模型的无量纲化定义的TFR随着分岔参数[公式:见正文]经历霍普夫分岔,其中[公式:见正文]是线粒体分裂因子(Mff)的总浓度,k +和k -是线粒体外膜上寡聚体之间的缔合和解离速率常数。变量μ可以被认为是寡聚体拆卸速率上的最大生成速率。虽然系统的无量纲化产生了四个无量纲参数,但我们发现TFR和累积总分裂(TF)仅强烈依赖于一个参数,即μ。有趣的是,累积TF并不随着μ的增加而单调增加。相反,它随着μ增加到某一点,然后随着μ继续增加而开始下降。这种对μ的非单调依赖性表明,针对k +、k -或[公式:见正文]的干预可能对分裂机制产生非直观的影响。因此,了解诸如μ等调节参数的影响可能有助于未来治疗靶点的选择。