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Biology subjects

Simpson, E.

Publications and source records attributed to Simpson, E..

4 recordsLinked to original sources

The impact of coinfection on population stability and chaos

Parasites play an outsized role in mediating the persistence and stability of host populations. Flour beetles (Tribolium spp.) have long served as classic examples of population dynamics under both disease-free and infected conditions, with elegant combinations of theory and experiments demonstrating, for example, that cannibalism rates can push populations from stability to chaos. As with most organisms in nature, however, flour beetles rarely face just one parasite species, and co-infecting parasites can antagonize or facilitate each other through resources and immunity. To test the prediction that non-neutral interactions would qualitatively alter population stability, we first raised flour beetles (Tribolium castaneum) in infection-free, single-infection, or coinfection microcosms and quantified relative prevalence and parasite intensity. Next, we reworked a classic stage-structured discrete-time model to include single and multiple infections and performed sensitivity and bifurcation analyses to identify the most important (co)infection-associated parameters for population stability. The model predicts that stability is highly sensitive to parasite transmission mode regardless of infection multiplicity, but facilitation among parasites rapidly drives populations into oscillations and chaos under realistic conditions. This study identifies an important mechanism for explaining population variability and highlights the importance of within-host mechanisms for driving dynamics at higher levels of biological organization.

ecology↗

A controlled environment assay for the rapid evaluation of verticillium stripe resistance in canola

Verticillium stripe disease is an emerging threat to canola production in Western Canada. Accurately assessing verticillium stripe resistance in breeding germplasm collections is crucial for identifying sources of genetic resistance. Currently, field phenotyping is the most widely used method for evaluating verticillium stripe resistance; however, achieving uniform disease pressure under field conditions presents significant challenges. Here we report a novel controlled environment (CE) soil-less assay for the rapid evaluation of verticillium stripe resistance in canola. The CE results were validated in a field trial which showed a strong correlation between the field data and the CE results. This cost-effective and time-efficient assay enables accurate assessment of verticillium stripe symptoms in a one-month testing cycle.

pathology↗

Drivers of individual plant species contributions to β-diversity are scale-dependent

Species introductions and native extirpations are driving biotic homogenisation in plant communities by reducing {beta}-diversity. Individual species vary in their contributions to {beta}-diversity (Species Contribution to {beta}-Diversity; species-{beta}), yet our understanding of how species characteristics shape these contributions remains limited. Additionally, although the ecological processes influencing {beta}-diversity are known to vary with spatial scale, we lack understanding of how species contributions, or their underlying determinants, change across scales. Here, we modelled how plant functional traits, phylogenetic relatedness, and introduction status influence their contributions to {beta}-diversity using plant community data from 429 plots surveyed from 2017-2023 across three nested spatial scales (up to 1 km2) in nine sites spanning four countries. We extended the analysis to broader spatial extents (100 km2 to the entire UK) using GBIF occurrence data. We found that functional traits associated with competitive ability influenced species-{beta}, but the direction and strength of their effects varied with scale. Likewise, phylogenetic novelty increased species-{beta} at small scales but reduced it at larger ones. After accounting for traits and phylogeny, introduced species consistently contributed less to {beta}-diversity than native species--especially at broader spatial extents. These results demonstrate that species ecological and evolutionary characteristics shape their contributions to {beta}-diversity, but that these effects are scale-dependent. Our findings highlight the importance of scale-explicit approaches in understanding both the determinants of {beta}-diversity, and how we can combat its loss to mitigate biotic homogenisation.

ecology↗

SARS-CoV-2 Viral Genes Compromise Survival and Functions of Human Pluripotent Stem Cell-derived Cardiomyocytes via Reducing Cellular ATP Level

Cardiac manifestations are commonly observed in COVID-19 patients and prominently contributed to overall mortality. Human myocardium could be infected by SARS-CoV-2, and human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) are susceptible to SARS-CoV-2 infection. However, molecular mechanisms of SARS-CoV-2 gene-induced injury and dysfunction of human CMs remain elusive. Here, we find overexpression of three SARS-CoV-2 coding genes, Nsp6, Nsp8 and M, could globally compromise transcriptome of hPSC-CMs. Integrated transcriptomic analyses of hPSC-CMs infected by SARS-CoV-2 with hPSC-CMs of Nsp6, Nsp8 or M overexpression identified concordantly activated genes enriched into apoptosis and immune/inflammation responses, whereas reduced genes related to heart contraction and functions. Further, Nsp6, Nsp8 or M overexpression induce prominent apoptosis and electrical dysfunctions of hPSC-CMs. Global interactome analysis find Nsp6, Nsp8 and M all interact with ATPase subunits, leading to significantly reduced cellular ATP level of hPSC-CMs. Finally, we find two FDA-approved drugs, ivermectin and meclizine, could enhance the ATP level, and ameliorate cell death and dysfunctions of hPSC-CMs overexpressing Nsp6, Nsp8 or M. Overall, we uncover the global detrimental impacts of SARS-CoV-2 genes Nsp6, Nsp8 and M on the whole transcriptome and interactome of hPSC-CMs, define the crucial role of ATP level reduced by SARS-CoV-2 genes in CM death and functional abnormalities, and explore the potentially pharmaceutical approaches to ameliorate SARS-CoV-2 genes-induced CM injury and abnormalities.

molecular biology↗