Local clock models propose that the rate of molecular evolution is constant within phylogenetic sub-trees. Current local clock inference procedures scale poorly to large taxa problems, impose model misspecification, or require a priori knowledge of the existence and location of clocks. To overcome these challenges, we present an autocorrelated, Bayesian model of heritable clock rate evolution that leverages heavy-tailed priors with mean zero to shrink increments of change between branch-specific clocks. We further develop an efficient Hamiltonian Monte Carlo sampler that exploits closed form gradient computations to scale our model to large trees. Inference under our shrinkage-clock exhibits an over 3-fold speed increase compared to the popular random local clock when estimating branch-specific clock rates on a simulated dataset. We further show our shrinkage-clock recovers known local clocks within a rodent and mammalian phylogeny. Finally, in a problem that once appeared computationally impractical, we investigate the heritable clock structure of various surface glycoproteins of influenza A virus in the absence of prior knowledge about clock placement.
翻译:本地时钟模型显示,分子进化速度在植物遗传亚树中是恒定的。 当前的本地时钟推导程序对大型分类问题来说不甚理想, 造成模型错误区分, 或者需要先验地了解钟的存在和位置。 为了克服这些挑战, 我们提出了一个与自动有关的巴耶斯时钟进化模型, 利用重尾前科, 平均为零, 以缩小分支时钟之间变化的增速。 我们进一步开发一个高效的汉密尔顿·蒙特·卡洛取样器, 利用封闭式梯度计算方法将模型扩大到大树。 我们的收缩时钟显示, 在估算模拟数据集中特定时钟速时速时速时速时速时速时速比流行的当地时钟速速度增加了3倍以上。 我们进一步展示我们的缩时钟模型在鼠标和哺乳动物时速中恢复了已知的当地时钟。 最后, 在一个一旦出现计算不切实际的问题中, 我们调查各种流感病毒表面蛋白质的时钟结构, 之前没有关于时钟的位置的知识。