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Biology subjects

Skelly, D. K.

Publications and source records attributed to Skelly, D. K..

3 recordsLinked to original sources

Gene Flow and Recent Lineage Colonization Constrain Genetic Differentiation Despite Local Adaptation

Demographic processes such as colonization to new environments and gene flow fundamentally shape the genomic landscape, either facilitating or constraining the efficiency of selection by altering the balance between genetic diversity and adaptive responses. Although theoretical predictions suggest that the efficacy of selection is dictated by a species' demographic history, empirical studies often overlook these constraints, yielding misleading observations. In this study, we present the first functional genome annotation for the wood frog (Lithobates sylvaticus), providing a critical genomic resource for understanding the adaptive capacity of the species. Based on the annotation, we examined the potential for selection to drive genomic and phenotypic divergence among populations distributed across vernal ponds in Northeastern Connecticut, USA. A genotypexenvironment association analysis revealed that the frequency of an outlier loci (Rab28) spikes in response to one wetland that is notable for having relatively low canopy cover and large area. We also found that selection has driven a strong disparity in embryonic development among populations of wood frog at a rate exceeding that of neutral genetic drift. This genomic signature of selection together with a remarkable phenotypic differentiation suggests that natural selection overcomes the power of genetic drift, even in a landscape characterized by relatively recent colonization and substantial evidence of connectivity among breeding wetlands. These findings improve our understanding of the wood frog's variation at a microgeographic scale.

evolutionary biology↗

A shared pathogen reservoir can tip widespread infection into mass mortality

Pathogens that persist subclinically across many wildlife populations can drive mass mortality in others. Mass mortality is often abrupt, and the timing can be difficult to predict from host or habitat features alone. In a recent field study tracking ranavirus epizootics in wood frog (Rana sylvatica) breeding ponds, we found that no environmental or biotic feature reliably predicted die-off occurrence or timing. Instead, the trajectory of viral accumulation in the water column was the strongest dynamic predictor of mass mortality. Infected hosts shed virus throughout epizootics, but the influence of waterborne viral concentration on disease progression was apparent only near die-off onset. This pattern suggests a potential threshold-dependent feedback operating through the shared viral environment. Here, we develop a compartmental model linking waterborne viral concentration to the rate at which subclinical infections progress to clinical, high-shedding states within already-infected hosts. We show that a dose-dependent progression model generates the two-phase epizootic trajectory observed in natural die-offs: prolonged subclinical circulation followed by abrupt clinical transition after environmental virus crosses an escalation threshold. The model exhibits a sharp phase transition between subclinical circulation and mass mortality, governed mainly by the clinical-to-subclinical shedding ratio, host density, and pond volume. Existing explanations for die-off variation emphasize individual-level susceptibility, but our model demonstrates that dose-dependent environmental feedback, a mechanism not previously formalized at the population level, can generate the transition from subclinical infection to mass mortality without invoking individual variation in host susceptibility. This mechanism may apply in any system where hosts share a bounded environment, pathogen dose influences disease severity, and pathogen shedding increases with disease progression.

ecology↗

Epizootic tipping points: Environmental viral feedbacks predict amphibian die-offs

Virulent pathogens commonly circulate in wildlife populations without causing mass mortality, but the processes driving die-offs remain poorly understood. Prevailing frameworks emphasize individual-level susceptibility, although susceptibility factors often fail to predict population-level outcomes. We tracked ranavirus epizootics across 40 wood frog breeding ponds over three years, comparing models based on lagged viral state variables with those based on abiotic and host conditions. Models based on lagged viral-state variables received greater support for subsequent infection spread, intensification, and viral accumulation. Prevalence predicted later environmental viral concentration throughout epizootics, whereas relationships between environmental viral concentration and subsequent infection spread and intensification were substantially weakened when die-off onsets were excluded, consistent with phase-dependent feedback. Viral accumulation rates differentiated die-off from non-die-off pond-years while static pond and host features did not, suggesting that die-offs may be associated with pathogen accumulation in shared environments rather than being predictable from static pond and host features alone.

ecology↗