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Biology subjects

Ellner, S.

Publications and source records attributed to Ellner, S..

3 recordsLinked to original sources

A time for every purpose: using time-dependent sensitivity analysis to help understand and manage dynamic ecological systems

Sensitivity analysis is often used to help understand and manage ecological systems, by assessing how a constant change in vital rates or other model parameters might affect the management outcome. This allows the manager to identify the most favorable course of action. However, realistic changes are often localized in time--for example, a short period of culling leads to a temporary increase in the mortality rate over the period. Hence, knowing when to act may be just as important as knowing what to act upon. In this article, we introduce the method of time-dependent sensitivity analysis (TDSA) that simultaneously addresses both questions. We illustrate TDSA using three case studies: transient dynamics in static disease transmission networks, disease dynamics in a reservoir species with seasonal life-history events, and endogenously-driven population cycles in herbivorous invertebrate forest pests. We demonstrate how TDSA often provides useful biological insights, which are understandable on hindsight but would not have been easily discovered without the help of TDSA. However, as a caution, we also show how TDSA can produce results that mainly reflect uncertain modeling choices and are therefore potentially misleading. We provide guidelines to help users maximize the utility of TDSA while avoiding pitfalls.

ecology↗

Modeling phytoplankton-zooplankton interactions: opportunities for species richness and challenges for modern coexistence theory

Many potential mechanisms can sustain biodiversity, but we know little about their relative importance. To compare multiple mechanisms, we modeled a two-trophic planktonic food-web based on mechanistic species interactions and empirically measured species traits. We simulated thousands of communities under realistic and altered trait distributions to assess the relative importance of three potential drivers of species richness: resource competition, predator-prey interactions, and trait trade-offs. Next, we computed niche and fitness differences of competing zooplankton to obtain a deeper understanding of how these mechanisms limit species richness. We found that predator-prey interactions were the most important driver of species richness and that fitness differences were a better predictor of species richness than niche differences. However, for many communities we could not apply modern coexistence theory to compute niche and fitness differences due to complications arising from trophic interactions. We therefore need to expand modern coexistence theory to investigate multi-trophic communities.

ecology↗

Host-pathogen Immune Feedbacks Can Explain Widely Divergent Outcomes from Similar Infections

A longstanding question in infection biology is why two very similar individuals, with very similar pathogen exposures, may have very different outcomes. Recent experiments have found that even isogenic Drosophila melanogaster hosts, given identical inoculations of some bacterial pathogens at suitable doses, can experience very similar initial bacteria proliferation but then diverge to either a lethal infection or a sustained chronic infection with much lower pathogen load. We hypothesized that divergent infection outcomes are a natural result of mutual negative feedbacks between pathogens and the host immune response. Here we test this hypothesis in silico by constructing process-based dynamic models for bacterial population growth, host immune induction, and the feedbacks between them, based on common mechanisms of immune system response. Mathematical analysis of a minimal conceptual model confirms our qualitative hypothesis that mutual negative feedbacks can magnify small differences among hosts into life-or-death differences in outcome. However, explaining observed features of chronic infections requires an extension of the model to include induced pathogen modifications that shield themselves from host immune responses at the cost of reduced proliferation rate. Our analysis thus generates new, testable predictions about the mechanisms underlying bimodal infection outcomes.

systems biology↗