Non-Poissonian Bursts in the Arrival of Phenotypic Variation Can Strongly Affect the Dynamics of Adaptation
Molecular Biology and Evolution Oxford University Press 41:6 (2024) msae085
Abstract:
Modeling the rate at which adaptive phenotypes appear in a population is a key to predicting evolutionary processes. Given random mutations, should this rate be modeled by a simple Poisson process, or is a more complex dynamics needed? Here we use analytic calculations and simulations of evolving populations on explicit genotype–phenotype maps to show that the introduction of novel phenotypes can be “bursty” or overdispersed. In other words, a novel phenotype either appears multiple times in quick succession or not at all for many generations. These bursts are fundamentally caused by statistical fluctuations and other structure in the map from genotypes to phenotypes. Their strength depends on population parameters, being highest for “monomorphic” populations with low mutation rates. They can also be enhanced by additional inhomogeneities in the mapping from genotypes to phenotypes. We mainly investigate the effect of bursts using the well-studied genotype–phenotype map for RNA secondary structure, but find similar behavior in a lattice protein model and in Richard Dawkins’s biomorphs model of morphological development. Bursts can profoundly affect adaptive dynamics. Most notably, they imply that fitness differences play a smaller role in determining which phenotype fixes than would be the case for a Poisson process without bursts.Conformal field theory approach to parton fractional quantum Hall trial wave functions
Physical Review B American Physical Society (APS) 109:20 (2024) 205128
Entropy production and thermodynamic inference for stochastic microswimmers
Physical Review Research American Physical Society (APS) 6:2 (2024) l022044
Stress-shape misalignment in confluent cell layers
Nature Communications Nature Research 15:1 (2024) 3628
Abstract:
In tissue formation and repair, the epithelium undergoes complex patterns of motion driven by the active forces produced by each cell. Although the principles governing how the forces evolve in time are not yet clear, it is often assumed that the contractile stresses within the cell layer align with the axis defined by the body of each cell. Here, we simultaneously measured the orientations of the cell shape and the cell-generated contractile stresses, observing correlated, dynamic domains in which the stresses were systematically misaligned with the cell body. We developed a continuum model that decouples the orientations of contractile stress and cell body. The model recovered the spatial and temporal dynamics of the regions of misalignment in the experiments. These findings reveal that the cell controls its contractile forces independently from its shape, suggesting that the physical rules relating cell forces and cell shape are more flexible than previously thought.An exactly solvable model for emergence and scaling laws in the multitask sparse parity problem
(2024)