Microbial cells reprogram energy and protein metabolism in response to plastic exposure

Polypropylene plastic consumables, also known as metabolically inert materials, are commonly used in microbial biotechnology studies, but our understanding of their effects on microbial physiology and metabolism remains limited. Here we show that microbial growth in plastic differs metabolically from that in glass using Escherichia coli BL21 and Pichia pastoris GS115 as prokaryotic and eukaryotic model organisms, respectively. Exposure to polypropylene plastic significantly inhibits microbial growth, as evidenced by an extended lag phase and dramatic reductions in biomass. We observed that polypropylene plastic induces a 3.6-fold increase in intracellular reactive oxygen species levels in BL21 and a 7.9-fold increase in GS115, independent of dissolved oxygen availability. This led to the repression of central carbon metabolism, including glycolysis, the TCA cycle, and oxidative phosphorylation, as evidenced by intracellular acetyl-CoA levels decreasing by 7.6-fold in BL21 and 7.5-fold in GS115, and by a concomitant reduction in ATP availability. Conversely, a significant enhancement of ribosome biogenesis and protein processing decouples energy metabolism from protein synthesis, leading to an 8.0-fold increase in total protein content in GS115 and a 5.3-fold increase in BL21. Comparative transcriptomic and LC–MS/MS profiling revealed that plastic affects microbial metabolism through surface interactions rather than leached agents. Collectively, our findings provide a significant conceptual advance on microbial responses to plastic exposure, informing biotechnology and/or biochemical studies in plastic environments.