@article{21322, abstract = {Habitat fragmentation poses a significant risk to population survival, causing both demographic stochasticity and genetic drift within local populations to increase, thereby increasing genetic load. Higher load causes population numbers to decline, which reduces the efficiency of selection and further increases load, resulting in a positive feedback that may drive entire populations to extinction. Here, we investigate this eco-evolutionary feedback in a metapopulation consisting of local demes connected via migration, with individuals subject to deleterious mutation at a large number of loci. We first analyze the determinants of load under soft selection, where population sizes are fixed, and then build on this to understand hard selection, where population sizes and load coevolve. We show that under soft selection, very little gene flow (less than one migrant per generation) is enough to prevent fixation of deleterious alleles. By contrast, much higher levels of migration are required to mitigate load and prevent extinction when selection is hard, with critical migration thresholds for metapopulation persistence increasing sharply as the genome-wide deleterious mutation rate becomes comparable to the baseline population growth rate. Moreover, critical migration thresholds are highest if deleterious mutations have intermediate selection coefficients but lower if alleles are predominantly recessive rather than additive (due to more efficient purging of recessive load within local populations). Our analysis is based on a combination of analytical approximations and simulations, allowing for a more comprehensive understanding of the factors influencing load and extinction in fragmented populations.}, author = {Olusanya, Oluwafunmilola O and Khudiakova, Kseniia and Sachdeva, Himani}, issn = {1537-5323}, journal = {The American Naturalist}, number = {6}, pages = {617--636}, publisher = {University of Chicago Press}, title = {{Genetic load, eco-evolutionary feedback, and extinction in metapopulations}}, doi = {10.1086/735562}, volume = {205}, year = {2025}, } @article{20056, abstract = {Theoretical studies have shown that stochasticity can affect the dynamics of ecosystems in counterintuitive ways. However, without knowing the equations governing the dynamics of populations or ecosystems, it is difficult to ascertain the role of stochasticity in real datasets. Therefore, the inverse problem of inferring the governing stochastic equations from datasets is important. Here, we present an equation discovery methodology that takes time series data of state variables as input and outputs a stochastic differential equation. We achieve this by combining traditional approaches from stochastic calculus with the equation discovery techniques. We demonstrate the generality of the method via several applications. First, we deliberately choose various stochastic models with fundamentally different governing equations, yet they produce nearly identical steady-state distributions. We show that we can recover the correct underlying equations, and thus infer the structure of their stability, accurately from the analysis of time series data alone. We demonstrate our method on two real-world datasets—fish schooling and single-cell migration—that have vastly different spatiotemporal scales and dynamics. We illustrate various limitations and potential pitfalls of the method and how to overcome them via diagnostic measures. Finally, we provide our open-source code via a package named PyDaDDy (Python Library for Data-Driven Dynamics).}, author = {Nabeel, Arshed and Karichannavar, Ashwin and Palathingal, Shuaib and Jhawar, Jitesh and Brückner, David and Raj M, Danny and Guttal, Vishwesha}, issn = {1537-5323}, journal = {The American Naturalist}, number = {4}, pages = {E100--E117}, publisher = {University of Chicago Press}, title = {{Discovering stochastic dynamical equations from ecological time series data}}, doi = {10.1086/734083}, volume = {205}, year = {2025}, } @article{3393, abstract = {Unlike unconditionally advantageous “Fisherian” variants that tend to spread throughout a species range once introduced anywhere, “bistable” variants, such as chromosome translocations, have two alternative stable frequencies, absence and (near) fixation. Analogous to populations with Allee effects, bistable variants tend to increase locally only once they become sufficiently common, and their spread depends on their rate of increase averaged over all frequencies. Several proposed manipulations of insect populations, such as using Wolbachia or “engineered underdominance” to suppress vector-borne diseases, produce bistable rather than Fisherian dynamics. We synthesize and extend theoretical analyses concerning three features of their spatial behavior: rate of spread, conditions to initiate spread from a localized introduction, and wave stopping caused by variation in population densities or dispersal rates. Unlike Fisherian variants, bistable variants tend to spread spatially only for particular parameter combinations and initial conditions. Wave initiation requires introduction over an extended region, while subsequent spatial spread is slower than for Fisherian waves and can easily be halted by local spatial inhomogeneities. We present several new results, including robust sufficient conditions to initiate (and stop) spread, using a one-parameter cubic approximation applicable to several models. The results have both basic and applied implications.}, author = {Barton, Nicholas H and Turelli, Michael}, issn = {1537-5323}, journal = {American Naturalist}, number = {3}, pages = {E48 -- E75}, publisher = {The University of Chicago Press}, title = {{Spatial waves of advance with bistable dynamics: Cytoplasmic and genetic analogues of Allee effects}}, doi = {10.1086/661246}, volume = {178}, year = {2011}, } @article{3659, abstract = {We develop models of the rates of evolution at sex-linked and autosomal loci and of the rates of fixation of chromosomal rearrangements involving sex chromosomes and autosomes. We show that the substitution of selectively favorable mutations often proceeds more rapidly for X- or Y-linked loci than for the autosomes, provided that mutations are recessive or partially recessive on the average. Selection acting on a quantitative character is expected to result in similar long-term rates of gene substitution for X-linked and autosomal loci, unless there is strong directional dominance. Short-term responses to such selection often preferentially fix alleles at autosomal loci. The fixation of slightly deleterious alleles by random drift and the stochastic turnover of alleles at loci controlling quantitative characters under stabilizing selection usually proceed somewhat more slowly at sex-linked loci. In contrast, the fixation of underdominant chromosomal rearrangements by random genetic drift is faster with sex linkage. Sex-specific selection may also differentially favor the fixation of sex-linked rearrangements. These results are discussed in relation to genetic and cytological data on species differences. We show that the frequently disproportionate effects of the sex chromosomes on interspecific inviability or sterility are consistent with the hypothesis that the gene differences concerned involve recessive or partially recessive alleles fixed by selection. Haldane's rule is readily interpreted in this light. There is little evidence for strong effects of the sex chromosomes on quantitative characters in interspecific crosses, in accordance with our theoretical results. Thus, the evolution of reproductive isolation may not be the byproduct of selective change in additively inherited, polygenic traits. Rather, it may be due mainly to the fixation of favorable mutations whose effects on fitness reflect locus-specific effects on the phenotype. These mutations behave as major genes in the sense of contributing the bulk of the genetic variance in the characters that they control during the course of the mutations' substitution. The data on the genetics of short-term responses to selection in Drosophila are hard to interpret, but, in accordance with theory, these responses do not usually seem to involve the X chromosome disproportionately. In some groups, there is evidence for a disproportionate role of the sex chromosomes in chromosomal changes, but others show no clear pattern. Factors that may distort the expectations of the simple models of chromosomal evolution are discussed.}, author = {Charlesworth, Brian and Coyne, Jerry and Barton, Nicholas H}, issn = {1537-5323}, journal = {American Naturalist}, number = {1}, pages = {113 -- 146}, publisher = {University of Chicago Press}, title = {{The relative rates of evolution of sex chromosomes and autosomes}}, doi = {10.1086/284701}, volume = {130}, year = {1987}, }