Collective decision making in bacterial viruses.
Collective decision making in bacterial viruses.
复制标题
细菌病毒的集体决策。
DOI：
10.1529/biophysj.108.133694
复制
发表时间：
2008
影响因子：
3.4
通讯作者：
E. Voit
中科院分区：
文献类型：
--
作者：
J. Weitz;Yuriy Mileyko;Richard I. Joh;E. Voit
对于许多细菌病毒来说，选择是杀死宿主细胞还是进入潜伏状态取决于合并感染的多样性。在这里，我们提出了一个关于细菌病毒如何对受感染细胞的命运做出集体决定的数学理论。我们的理论基础上的基因调控动力学的机制模型。与大多数以前的工作不同，我们将病毒基因的拷贝数视为变量。增加病毒拷贝数会增加病毒mRNA的转录速率。当病毒对细胞命运的调控包括非线性反馈回路时，转录速率的微小变化可导致稳态基因表达的显著变化。因此，我们证明了确定性决策可以达到，例如，裂解或潜伏期，这取决于病毒决策的基因调控模型中的细胞感染多样性。与温和的噬菌体λ的决定结构的分子研究的模型的参数化版本的比较与我们的结论是一致的。由于该模型是通用的，它表明，细菌病毒可以适应性地响应种群动态的变化，并在病毒的集体决策的功能是可进化的生活史特征。
For many bacterial viruses, the choice of whether to kill host cells or enter a latent state depends on the multiplicity of coinfection. Here, we present a mathematical theory of how bacterial viruses can make collective decisions concerning the fate of infected cells. We base our theory on mechanistic models of gene regulatory dynamics. Unlike most previous work, we treat the copy number of viral genes as variable. Increasing the viral copy number increases the rate of transcription of viral mRNAs. When viral regulation of cell fate includes nonlinear feedback loops, very small changes in transcriptional rates can lead to dramatic changes in steady-state gene expression. Hence, we prove that deterministic decisions can be reached, e.g., lysis or latency, depending on the cellular multiplicity of infection within a broad class of gene regulatory models of viral decision-making. Comparisons of a parameterized version of the model with molecular studies of the decision structure in the temperate bacteriophage lambda are consistent with our conclusions. Because the model is general, it suggests that bacterial viruses can respond adaptively to changes in population dynamics, and that features of collective decision-making in viruses are evolvable life history traits.
影响因子：
3.4
作者：
Bennett, Matthew R.;Volfson, Dmitri;Hasty, Jeff
通讯作者：
Hasty, Jeff
影响因子：
5.6
作者：
SHEA, MA;ACKERS, GK
通讯作者：
ACKERS, GK