Adaptive resistance and defense evolution in microplastics-mediated biological exposure interfaces in municipal...

To test the hypothesis that microplastic (MP)-mediated BXI triggers quorum sensing (QS)-driven resistance evolution, we established a multilevel mechanism: interface biological exposure → structural/functional changes → functional gene enhancement → QS activation → resistance/defense evolution. The results confirm that three MP (PET, PE, and PP)-mediated biological exposures induce the overexpression of genes encoding extracellular polymeric substances (EPS), stabilize microbial aggregates (proteins/enzymes), and promote BXI formation while reducing catalase/superoxide dismutase inhibition. MP exposure correlated with altered microbial communities, enriched stress resistance genera (Acinetobacter, Nitrospira, and Hyphomicrobium), and resulted in the formation of robust co-occurrence networks (73.53-90.67 % positive correlations). Enhanced QS signaling (AI-2, DSF, and c-di-GMP) upregulated autoinducer/transporter genes, accelerating EPS synthesis and energy metabolism. MP-mediated BXI strengthens microbial resilience and nitrogen/sulfur cycle equilibrium via organic carbon degradation, nitrification-denitrification enhancement, and sulfite/thiosulfate oxidation, whereas protein-enzyme synergy improves pollutant resilience. Through signal compensation and pathway adaptation, microbial communities stabilize BXI under MP stress. These findings provide novel insights into the in situ control of MP-driven pollutant migration in MWTS.