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The Paradoxical Toxicity of Microplastics under Predation Risk: The Driving Role of Gut Microbiota-Mediated Tolerance
Summary
Researchers found that Daphnia clones adapted to fish predation were significantly more tolerant to combined microplastic and predation stress than predator-naive clones, and demonstrated through microbiota transplant experiments that this tolerance was causally driven by the adapted gut microbiome's enrichment in carbohydrate metabolism and immune defense functions.
genotypes revealed that the fish-adapted clone exhibited superior tolerance to combined exposure to stressors, maintaining robust growth and defensive integrity, unlike the fish-naïve clone. The gut microbiome was identified as a key mechanistic driver. The fish-adapted clone maintained a more stable microbial community structure with functions enriched in carbohydrate metabolism and immune defense. A reciprocal transplantation experiment provided causal evidence: transplanting the adapted microbiota into the predator-naïve clone reduced mortality by 39% and increased intrinsic growth by 22% under combined stress. These findings highlight that microplastics risk assessment may be flawed if they ignore the eco-evolutionary context of natural stressors.