Biology subjects

Alfaro, M.

Publications and source records attributed to Alfaro, M..

4 recordsLinked to original sources

bioRxiv2022

Evolution and spread of multidrug resistant pathogens in a spatially heterogeneous environment

The emergence and the spread of multi-adapted pathogens is often viewed as a slow process resulting from the incremental accumulation of single adaptations. In bacteria, for instance, multidrug resistance to antibiotics may result from the sequential acquisition of single drug resistance to different antibiotics. In phytopathogens, the ability to infect different resistant varieties of crops may also result from the accumulation of distinct virulence genes. Here we use a general epidemiological model to analyse the evolution of pathogen adaptations throughout an epidemic spreading in a heterogeneous host population where selection varies periodically in space. This spatially heterogeneous selection may result from the use of different drugs, different vaccines or different crop varieties in agriculture. We study both the transient evolution of pathogen adaptation at the front of the epidemic and the long-term evolution far behind the epidemic front. We identify five different types of epidemic profiles that may arise from different combinations of spatial heterogeneity and the cost of multi-adaptation. In particular, we show that multi-adaptation can drive epidemic spread, while the evolution of single-adaptation may only occur in a second phase, when the pathogen specializes on local selective pressures. Indeed, a generalist pathogen with multiple adaptations can outpace the spread of a coalition of specialist pathogens when selection varies frequently in space. This result is amplified in finite host populations because demographic stochasticty can lead to the extinction of maladapted pathogens specialised to a local selective pressure. Our work has important implications for the management of multiple drugs and vaccines against pathogens but also for the optimal deployment of resistant varieties in agriculture.

evolutionary biology↗

bioRxiv2022

Considering decoupled phenotypic diversification between ontogenetic phases in macroevolution: An example using Triggerfishes (Balistidae)

Across the Tree of Life, most studies of phenotypic disparity and diversification have been restricted to adult organisms. However, many lineages have distinct ontogenetic phases that do not reflect the same traits as their adult forms. Non-adult disparity patterns are particularly important to consider for coastal ray-finned fishes, which often have juvenile phases with distinct phenotypes. These juvenile forms are often associated with sheltered nursery environments, with phenotypic shifts between adults and juvenile stages that are readily apparent in locomotor morphology. However, whether this ontogenetic variation in locomotor morphology reflects a decoupling of diversification dynamics between life stages remains unknown. Here we investigate the evolutionary dynamics of locomotor morphology between adult and juvenile triggerfishes. Integrating a time-calibrated phylogenetic framework with geometric morphometric approaches and measurement data of fin aspect ratio and incidence, we reveal a mismatch between morphospace occupancy, the evolution of morphological disparity, and the tempo of trait evolution between life stages. Collectively, our results illuminate how the heterogeneity of morpho-functional adaptations can decouple the mode and tempo of morphological diversification between ontogenetic stages.

evolutionary biology↗

bioRxiv2021

The emergence of a birth-dependent mutation rate in asexuals: causes and consequences

AO_SCPLOWBSTRACTC_SCPLOWIn unicellular organisms such as bacteria and in most viruses, mutations mainly occur during reproduction. Thus, genotypes with a high birth rate should have a higher mutation rate. However, standard models of asexual adaptation such as the replicator-mutator equation often neglect this generation-time effect. In this study, we investigate the emergence of a positive dependence between the birth rate and the mutation rate in models of asexual adaptation and the consequences of this dependence. We show that it emerges naturally at the population scale, based on a large population limit of a stochastic time-continuous individual-based model with elementary assumptions. We derive a reaction-diffusion framework that describes the evolutionary trajectories and steady states in the presence of this dependence. When this model is coupled with a phenotype to fitness landscape with two optima, one for birth, the other one for survival, a new trade-off arises in the population. Compared to the standard approach with a constant mutation rate, the symmetry between birth and survival is broken. Our analytical results and numerical simulations show that the trajectories of mean phenotype, mean fitness and the stationary phenotype distribution are in sharp contrast with those displayed for the standard model. The reason for this is that the usual weak selection limit does not hold in a complex landscape with several optima associated with different values of the birth rate. Here, we obtain trajectories of adaptation where the mean phenotype of the population is initially attracted by the birth optimum, but eventually converges to the survival optimum, following a hook-shaped curve which illustrates the antagonistic effects of mutation on adaptation.

evolutionary biology↗

bioRxiv2019

On the effect of asymmetrical trait inheritance on models of trait evolution

Current phylogenetic comparative methods modeling quantitative trait evolution generally assume that, during speciation, phenotypes are inherited identically between the two daughter species. This, however, neglects the fact that species consist of a set of individuals, each bearing its own trait value. Indeed, because descendent populations after speciation are samples of a parent population, we can expect their mean phenotypes to randomly differ from one another potentially generating a "jump" of mean phenotypes due to asymmetrical trait inheritance at cladogenesis. Here, we aim to clarify the effect of asymmetrical trait inheritance at speciation on macroevolutionary analyses, focusing on model testing and parameter estimation using some of the most common models of quantitative trait evolution. We developed an individual-based simulation framework in which the evolution of species phenotypes is determined by trait changes at the individual level accumulating across generations and cladogenesis occurs then by separation of subsets of the individuals into new lineages. Through simulations, we assess the magnitude of phenotypic jumps at cladogenesis under different modes of trait inheritance at speciation. We show that even small jumps can strongly alter both the results of model selection and parameter estimations, potentially affecting the biological interpretation of the estimated mode of evolution of a trait. Our results call for caution when interpreting analyses of trait evolution, while highlighting the importance of testing a wide range of alternative models. In the light of our findings, we propose that future methodological advances in comparative methods should more explicitly model the intra-specific variability around species mean phenotypes and how it is inherited at speciation.

evolutionary biology↗