Vulliet, E. | bioRxiv Science

bioRxiv2026

From urban runoff to mosquito success : spatiotemporal microbial assembly in larval water habitats under anthropogenic stressors

Urban mosquito habitats are heterogeneous aquatic ecosystems where anthropogenic inputs shape physicochemical conditions and microbial community assembly. However, the combined effects of environmental chemistry and microbial dynamics on mosquito fitness remain poorly understood across space and time. Here, we integrated environmental chemistry, metabarcoding, and experimental assays to investigate how spatiotemporal variation in urban larval habitats influences environmental microbial assembly and the biology of the Asian tiger mosquito, Aedes albopictus. Six stormwater drains were monitored over five months to characterize ions, dissolved gases, micropollutants, and bacterial and fungal communities. Laboratory assays using water from three contrasting habitats were then conducted to evaluate oviposition preference and mosquito performance. Microbial community composition was strongly structured by breeding-site identity and associated with distinct physicochemical signatures. Bacterial communities remained relatively stable over time, whereas fungal assemblages exhibited stronger temporal turnover. These environmental differences translated into marked variation in larval performance, ranging from rapid development and high survival to delayed development, reduced survival, and episodic cohort collapse under environmentally unstable conditions. Adult traits further revealed carry-over effects of larval environment exposure across life stages. Correlation analyses showed that mosquito fitness was associated with both abiotic variables and microbial taxa linked to larval survival, development, emergence, and adult longevity. In contrast, oviposition preference remained consistently high across habitats despite strong differences in offspring performance, indicating a decoupling between habitat attractiveness and suitability. Overall, our results demonstrate that anthropogenic stressors shape microbial assembly in urban larval habitats, with cascading consequences for mosquito fitness and population dynamics.

ecology↗

bioRxiv2019

In vivo characterisation of the toxicological properties of DPhP, one of the main degradation product of aryl phosphate esters.

BackgroundAryl phosphate esters (APEs), a main class of organophosphorus ester molecules, are widely used and commonly present in the environment. Health hazards associated with these compounds remain largely unknown and the effects of diphenyl phosphate (DPhP), one of their most frequent derivatives in human samples, are poorly characterised. ObjectiveOur aim was to investigate whether DPhP per se may represent a more relevant marker of exposure to APEs and determine its potential deleterious biological effects in chronically exposed mice. MethodsConventional animals (FVB mice) were acutely (intravenous or oral gavage) or chronically (0.1 mg.mL-1, 1 mg.mL-1, 10 mg.mL-1 in drink water) exposed to relevant doses of DPhP or triphenyl phosphate (TPhP), one of its main precursors in the environment. Both molecules were measured in blood and other relevant tissues by liquid chromatography-mass spectrometry (LC-MS). Biological effects of chronic DPhP exposure were addressed through liver multi-omics analysis combining mRNA extraction and sequencing to high resolution LC-MS to determine the corresponding metabolic profile. Deep statistical exploration was performed to extract correlated information, guiding further physiological analyses (immunohistochemistry (IHC) and animal growth measurement). ResultsAcute and chronic exposure to DPhP led to significant levels of this molecule in blood and other tissues, an effect missing with TPhP. Multi-omics analysis confirmed the existence of biological effects of DPhP, even at a very low dose of 0.1 mg.mL-1 in drinking water. Chemical structural homology and pathway mapping demonstrated a clear reduction of the fatty-acid catabolic processes centred on acylcarnitine and mitochondrial {beta}-oxidation. Interestingly, mRNA expression confirmed and extended these observations by demonstrating at all tested doses the overall repression of genes involved in lipid catabolic processes and regulated by PPAR, a master regulator of {beta}-oxidation and its associated ketogenesis. IHC analysis confirmed the alteration of these pathways by showing a specific downregulation of Hmgcs2, a kernel target gene of PPAR, at all doses tested, and surprisingly, a strong reduction of the lipid droplet content only at the highest dose. Overall, DPhP absorption led to weight loss, which was significant using the highest dose. ConclusionsOur results suggest that in mice, the effects of chronic exposure to DPhP, even at a low dose, are not negligible. Fatty acid metabolism in the liver in particular is essential for controlling fast and feast periods with adverse consequences on the overall physiology. Therefore, the impact of DPhP on circulating fat, cardiovascular and metabolic disease incidence deserves, in light of our results, further investigations.

pharmacology and toxicology↗