Biology subjects

Uricchio, L. H.

Publications and source records attributed to Uricchio, L. H..

10 recordsLinked to original sources

bioRxiv2026

Fitness landscapes for species interactions: when do population genetics and adaptive dynamics diverge?

Multiple frameworks have been developed to investigate the evolution of species interactions on fitness landscapes, each with unique strengths and weaknesses. These include adaptive dynamics, which uses linear stability analyses to predict eco-evolutionary outcomes resulting from the invasion of rare mutants into a resident population, and population genetics, which mechanistically models finite populations and stochastic processes in finite time. Though there are some known correspondences between these frameworks, it is not clear that they will always result in the same eco-evolutionary outcomes. Moreover, while adaptive dynamics is very powerful for predicting outcomes, it is not always straightforward to relate these predictions to the data generated in experimental evolution studies. Here, we use a data-driven model of microbial species interactions to compare and contrast the predictions of population genetics and adaptive dynamics. We derive expected outcomes for one-species and two-species evolutionary trajectories by using the invasion fitness landscape concept from adaptive dynamics, and then use analytical theory and forward-in-time simulations to set these predictions within the context of population genetic models. In the context of our one-species models, we show that the timescale of evolution depends on mutation supply and effect sizes, when populations are initialized both along and off a trade-off function. For two-species competition models, we show that mutation supply, effect sizes, and asymmetries between competing species result in discrepancies between adaptive dynamics and population genetics, especially in cases where adaptive dynamics predicts stable coexistence. Our study provides insight into the role of finite timescales, mutation supplies and population sizes in the evolution of species interactions, and facilitates further research that leverages the invasion fitness landscape concept within the realm of population genetics.

evolutionary biology↗

bioRxiv2023

A phylogenomic perspective on interspecific competition

Evolutionary processes may have substantial impacts on community assembly, but evidence for phylogenetic relatedness as a determinant of interspecific interaction strength remains mixed. In this perspective, we consider a possible role for discordance between gene trees and species trees in the interpretation of phylogenetic signal in studies of community ecology. Modern genomic data show that the evolutionary histories of many taxa are better described by a patchwork of histories that vary along the genome rather than a single species tree. If a subset of genomic loci harbor trait-related genetic variation, then the phylogeny at these loci may be more informative of interspecific trait differences than the genome background. We develop a simple method to detect loci harboring phylogenetic signal and demonstrate its application through a proof of principle analysis of Penicillium genomes and pairwise interaction strength. Our results show that phylogenetic signal that may be masked genome-wide could be detectable using phylogenomic techniques and may provide a window into the genetic basis for interspecific interactions. Data & code accessibilityData and code for this project are freely available in the repository linked below and will be permanently archived upon publication. Statement of authorshipNL, BEW, and LHU designed the research; NL performed experiments; NL and LHU performed computational analyses; NL, BEW, and LHU wrote the manuscript. Code repositoryhttps://github.com/uricchio/ILSComp

ecology↗

bioRxiv2022

Diurnality shapes the visual opsin genes of colorful Neotropical frogs

Amphibians are ideal for studying visual system evolution because their biphasic (aquatic and terrestrial) life history and ecological diversity expose them to a broad range of visual conditions. Here we evaluate signatures of selection on visual opsin genes across Neotropical anurans and focus on three diurnal clades that are well-known for the concurrence of conspicuous colors and chemical defense (i.e., aposematism): poison frogs (Dendrobatidae), Harlequin toads (Bufonidae: Atelopus), and pumpkin toadlets (Brachycephalidae: Brachycephalus). We found evidence of positive selection on 44 amino acid sites in LWS, SWS1, SWS2, and RH1 opsin genes, of which one in LWS and two in RH1 have been previously identified as spectral tuning sites in other vertebrates. Given that anurans have mostly nocturnal habits, the patterns of selection revealed new sites that might be important in spectral tuning for frogs, potentially for adaptation to diurnal habits and for color-based intraspecific communication. Furthermore, we provide evidence that SWS2, normally expressed in rod cells in amphibians, has likely been lost in the ancestor of Dendrobatidae, suggesting that under low-light levels, dendrobatids have inferior wavelength discrimination compared to other frogs. This loss might follow the origin of diurnal activity in dendrobatids and could have implications for their chemical ecology, biodiversity, and behavior. Our analyses show that assessments of opsin diversification in understudied groups could expand our understanding of the role of sensory system evolution in ecological adaptation.

evolutionary biology↗

bioRxiv2022

Multimodal disease transmission as a limiting factor for the spatial extent of a host plant

Theoretical models suggest that infectious diseases could play a substantial role in determining species ranges, but few studies have collected the empirical data required to test this hypothesis. Pathogens that sterilize their hosts or spread through frequency-dependent transmission could have especially strong effects on the limits of species distributions because sterilized hosts can serve as long-lived disease reservoirs and frequency-dependent transmission mechanisms are effective even at very low population densities. We collected spatial disease prevalence data and population abundance data for alpine carnations infected by the sterilizing pathogen M. violaceum, a disease that is spread through both frequency-dependent (vector-borne) and density-dependent (aerial spore transmission) mechanisms. Our 13-year study reveals rapid declines in population abundance without a compensatory decrease in disease prevalence. We apply a stochastic, spatial model of disease spread that accommodates spatial habitat heterogeneity to investigate how the population dynamics depend on multimodal (frequency-dependent and density-dependent) transmission. We found that the observed rate of population decline can be readily explained by multimodal transmission, but is unlikely to be explained by either frequency-dependent or density-dependent mechanisms alone. Multimodal disease transmission rates high enough to explain the observed decline predicted that eventual local extinction of the host species is highly likely. Our results add to a growing body of literature showing how multimodal transmission can constrain species distributions in nature. Open ResearchAll scripts associated with the analyses in this manuscript, as well as the data we collected, are available at https://github.com/uricchio/antherSmutDis.

ecology↗

bioRxiv2020

Understanding the emergence of contingent and deterministic exclusion in multispecies communities

Competitive exclusion can be classified as deterministic or as historically contingent. While competitive exclusion is common in nature, it has remained unclear when multispecies communities should be dominated by deterministic or contingent exclusion. Here, we provide a general theoretical approach to explain both the emergence and sources of competitive exclusion in multispecies communities. We illustrate our approach on an empirical competition system between annual and perennial plant species. First, we find that the life-history of perennial species increases the probability of observing contingent exclusion by increasing their effective intrinsic growth rates. Second, we find that the probability of observing contingent exclusion increases with weaker intraspecific competition, and not with the level of hierarchical competition. Third, we find a shift from contingent exclusion to dominance with increasing numbers of competing species. Our work provides a heuristic framework to increase our understanding about the predictability of species persistence within multispecies communities.

ecology↗

bioRxiv2019

Viruses rule over adaptation in conserved human proteins

Adaptive evolution often involves fast-evolving proteins, and the fastest-evolving proteins in primates include antiviral proteins engaged in an arms race with viruses 1-3. Even though fast-evolving antiviral proteins are the most studied cases of primate host adaptation against viruses, viruses predominantly interact with host proteins that are broadly conserved between distant species in order to complete their replication cycle 4. Broadly conserved proteins are generally viewed as playing a negligible role in adaptive evolution. Here, we used a dataset of ~4,500 human proteins known to physically interact with viruses (VIPs for Virus-Interacting Proteins), to test the involvement of broadly conserved proteins in adaptive evolution against viruses. We found that VIPs conserved between animals and fungi have experienced not only high rates of adaption, but also strong adaptive events. Broadly conserved proteins that do not interact with viruses experienced very little adaptation. As a result, the arms race with viruses explains more than 75% of adaptation in the most phylogenetically conserved subset of the human proteome. Our results imply that broadly conserved proteins have played a significant role in adaptation, and that viruses were likely one of very few selective pressures that were able to force the conserved, central pillars of host cellular functions to adapt during evolution.

evolutionary biology↗

bioRxiv2018

Exploiting selection at linked sites to infer the rate and strength of adaptation

Genomic data encodes past evolutionary events and has the potential to reveal the strength, rate, and biological drivers of adaptation. However, robust estimation of adaptation rate () and adaptation strength remains a challenging problem because evolutionary processes such as demography, linkage, and non-neutral polymorphism can confound inference. Here, we exploit the influence of background selection to reduce the fixation rate of weakly-beneficial alleles to jointly infer the strength and rate of adaptation. We develop a novel MK-based method (ABC-MK) to infer adaptation rate and strength, and estimate = 0.135 in human protein-coding sequences, 72% of which is contributed by weakly adaptive variants. We show that in this adaptation regime is reduced {approx} 25% by linkage genome-wide. Moreover, we show that virus-interacting proteins (VIPs) undergo adaptation that is both stronger and nearly twice as frequent as the genome average ( = 0.224, 56% due to strongly-beneficial alleles). Our results suggest that while most adaptation in human proteins is weakly-beneficial, adaptation to viruses is often strongly-beneficial. Our method provides a robust framework for estimating adaptation rate and strength across species.

evolutionary biology↗

bioRxiv2018

Exotic species dominate due to niche overlap in a complex grassland community

Niche and fitness differences control the outcome of competition, but determining their relative importance in invaded communities - which may be far from equilibrium - remains a pressing concern. Moreover, it is unclear whether classic approaches for studying competition, which were developed predominantly for pairs of interacting species, will fully capture dynamics in complex species assemblages. We parameterized a population dynamic model using competition experiments of two native and three exotic species from a grassland community. We found evidence for minimal fitness differences or niche differences between the native species, leading to slow replacement dynamics and priority effects, but large fitness advantages allowed exotics to unconditionally invade natives. Priority effects driven by strong interspecific competition between exotic species drove single-species dominance by one of two exotic species in 80% of model outcomes, while a complex mixture of non-hierarchical competition and coexistence between native and exotic species occurred in the remaining 20%. Fungal infection, a commonly hypothesized coexistence mechanism, had weak fitness effects, and is unlikely to substantially affect coexistence. In contrast to previous work on pairwise outcomes in largely native-dominated communities, our work supports a role for nearly-neutral dynamics and priority effects as drivers of species composition in invaded communities.

ecology↗

bioRxiv2017

Singleton Variants Dominate the Genetic Architecture of Human Gene Expression

The vast majority of human mutations have minor allele frequencies (MAF) under 1%, with the plurality observed only once (i.e., \"singletons\"). While Mendelian diseases are predominantly caused by rare alleles, their cumulative contribution to complex phenotypes remains largely unknown. We develop and rigorously validate an approach to jointly estimate the contribution of all alleles, including singletons, to phenotypic variation. We apply our approach to transcriptional regulation, an intermediate between genetic variation and complex disease. Using whole genome DNA and lymphoblastoid cell line RNA sequencing data from 360 European individuals, we conservatively estimate that singletons contribute ~25% of cis-heritability across genes (dwarfing the contributions of other frequencies). Strikingly, the majority (~76%) of singleton heritability derives from ultra-rare variants absent from thousands of additional samples. We develop a novel inference procedure to demonstrate that our results are consistent with rampant purifying selection shaping the regulatory architecture of most human genes.

evolutionary biology↗

bioRxiv2017

Evidence for evolutionary shifts in the fitness landscape of human complex traits

Selection and mutation shape genetic variation underlying human traits, but the specific evolutionary mechanisms driving complex trait variation are largely unknown. We developed a statistical method that uses polarized GWAS summary statistics from a single population to detect signals of mutational bias and selection. We found evidence for non-neutral signals on variation underlying several traits (BMI, schizophrenia, Crohns disease, educational attainment, and height). We then used simulations that incorporate simultaneous negative and positive selection to show that these signals are consistent with mutational bias and shifts in the fitness-phenotype relationship, but not stabilizing selection or mutational bias alone. We additionally replicate two of our top three signals (BMI and educational attainment) in an external cohort, and show that population stratification may have confounded GWAS summary statistics for height in the GIANT cohort. Our results provide a flexible and powerful framework for evolutionary analysis of complex phenotypes in humans and other species, and offer insights into the evolutionary mechanisms driving variation in human polygenic traits.\n\nImpact summaryMany traits are variable within human populations and are likely to have a substantial and complex genetic component. This implies that mutations that have a functional impact on complex human traits have arisen throughout our species evolutionary history. However, it remains unclear how processes such as natural selection may have acted to shape trait variation at the genetic and phenotypic level. Better understanding of the mechanisms driving trait variation could provide insights into our evolutionary past and help clarify why it has been so difficult to map the preponderance of causal variation for common heritable diseases.\n\nIn this study, we developed and applied methods for detecting signatures of mutation bias (i.e., the propensity of a new variant to be either trait-increasing or trait-decreasing) and natural selection acting on trait variation. We applied our approach to several heritable traits, and found evidence for both natural selection and mutation bias, including selection for decreased BMI and decreased risk for Crohns disease and schizophrenia.\n\nWhile our results are consistent with plausible evolutionary scenarios shaping a range of traits, it should be noted that the field of polygenic selection detection is still new, and current methods (including ours) rely on data from genome-wide association studies (GWAS). The data produced by these studies may be vulnerable to certain cryptic biases, especially population stratification, which could induce false selection signals. We therefore repeated our analyses for the top three hits in a cohort that should be less susceptible to this problem - we found that two of our top three signals replicated (BMI and educational attainment), while height did not. Our results highlight both the promise and pitfalls of polygenic selection detection approaches, and suggest a need for further work disentangling stratification from selection.

evolutionary biology↗