Host preference varies widely across mosquitoes, with many species feeding opportunistically on diverse vertebrate hosts, while others show strong fidelity to specific hosts. Anthropophilia, the behavioural preference for feeding on humans, is a defining characteristic of some mosquito species responsible for the transmission of major human diseases, including malaria, dengue, and yellow fever. The evolution of anthropophilia therefore has profound epidemiological implications because increased human biting elevates vectorial capacity and disease transmission potential. However, the ecological and evolutionary mechanisms driving this extreme specialisation has not yet been fully elucidated and remain difficult to unify across laboratory and field studies. Here we present an eco-evolutionary modelling framework that links genetically determined mosquito traits with spatially structured host environments. Our framework integrates innate olfactory sensitivity, blood meal-derived fitness benefits, and spatio-temporal host accessibility. Two complementary indices are introduced: a local specialisation index, capturing short-term ecological feeding strategies, and a co-evolutionary index, capturing long-term genetic coupling between host detection and resource utilisation. Our results demonstrate that host specialisation is not a default evolutionary outcome but an environmentally gated process, which is favoured in resource-poor or temporally varying habitats and strongly filtered by seasonality. The framework yields testable predictions regarding when specialisation emerges, persists, or collapses, with direct implications for predicting vector-borne disease risk in changing environments.
A. Sadykov, D. Sadykova, Tina Mukherjee et al.· bioRxiv· 0 citations
Multicellularity necessitated the evolution of cellular diversity and specialization, yet across organisms, the retention of cellular plasticity within defined physiological contexts is a recurring principle. Here, we examine early-diverging metazoans to reevaluate the evolutionary logic of stemness. Rather than viewing stem cells as exceptional, we argue that cellular plasticity represents a deeply conserved attribute of early life. The ability of cells to remain responsive, multipotent, and regenerative under ecological or physiological contexts challenges the notion of cellular identity. We integrate evidence across three layers: evolutionary origins of cellular plasticity, systemic physiological axes that govern stem cell behavior, and metabolic and epigenetic mechanisms that execute fate decisions. This synthesis reveals that stemness is not a default cellular state but a licensed state, permitted when organism-level physiological signals align with local tissue demands. Within this framework, regeneration, age-associated decline, and cancer emerge as evidence of how effectively systemic governance regulates cellular plasticity across multicellular life.
Jagriti Arora, Sakshi Tiwari, Dasaradhi Palakodeti et al.· Annual Review of Genetics· 0 citations
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