Integrated metagenomic and phosphorus fractionation analyses elucidate the mechanism driving soil phosphorus immobilization under erythromycin stress

Abstract

Erythromycin (EM) is widely detected in agroecosystems, yet its mechanistic impact on microbially driven soil phosphorus (P) cycling remains limited. Here, we integrated Hedley P fractionation with metagenomic sequencing in soil microcosms exposed to EM (0, 10, and 50 mg/kg) to track changes in P fractions, microbial community, and functional genetic potential. Our results revealed that EM caused significant P immobilization, reducing bioavailable P by 34.7-46.2% and active organic P by 22.8-24.3%, respectively, compared to the treatment without EM. This immobilization was also accompanied by a 12.14-20.61% decrease in acid and alkaline phosphatase activities. Concurrently, EM restructured the microbial community, specifically reducing key P-cycling genera such as Solirubrobacter, Gemmatimonas, Gaiella, and Blastococcus, while enriching Steroidobacter and Bacteroidota. Crucially, metagenomic analysis revealed that EM suppressed the core genes central to purine metabolism (purB, purH, purF, and purL), pyrimidine metabolism (phyH and nrdB/F), and pyruvate metabolism (pckG and ppdK), as well as the two-component regulatory system (SenX3 and RegX3). These suppression genes are significantly correlated with labile P pools, indicating a direct link between genetic perturbation and P bioavailability. Although EM increased alternative P-acquisition genes, such as gcd and phnA, this response appeared insufficient to compensate for the suppression of core P-cycling functions. Collectively, our findings indicate that EM exposure impairs soil P cycling by reducing core P-cycling genes and taxa, suppressing enzymatic P mineralization, and triggering compensatory responses. This link between suppressed microbial genes and impaired soil P cycling contributes to understanding how antibiotics may induce functional degradation.