Insights into adaptation mechanisms and survival strategies of Pseudomonas chlororaphis subsp. aurantiaca: A comparative proteomic study under PFOA exposure

Perfluorooctanoic acid (PFOA), increasingly detected at extreme concentrations in industrial hotspots, caused a reduction in growth and a prolonged lag phase in Pseudomonas chlororaphis subsp. aurantiaca . In order to reveal microbial adaptation mechanisms and survival strategies under exposure to PFOA, a comparative proteomic analysis was undertaken. The up-regulation of phosphoglycerol transferase, lipoproteins, and long-chain fatty acid synthesis, together with the down regulation of cis unsaturation of fatty acids and changes in specific membrane-embedded porins, indicate alterations in membrane structure, fluidity, and permeability. The up-regulation of the divalent cation–regulated outer membrane protein H1, accompanied by the down-regulation of zinc and other metal transporters, reflect changes in metal ion homeostasis. In particular, altered iron homeostasis and expression of iron-, Fe-S clusters-, and heme-containing proteins were detected, along with the reduced activity of some iron-containing enzymes, as a result of inhibition by PFOA. Up-regulated enzymes of the methylcitrate and the glyoxylate cycles indicate alterations in central metabolic pathways associated with lipid metabolism in PFOA-treated cells. Changes in the respiratory chain may influence enhanced superoxide radical formation, triggering increased ROS production and the up-regulation of antioxidant enzymes, except those involved in thiol-based redox processes. In addition, PFOA alters the regulation of virulence-associated proteins. • First proteomic study of P. chlororaphis from PFAS-contaminated site. • High PFOA exposure (500 ppm) altered outer membrane and metabolic processes. • PFOA suppressed defense and enhanced invasion-related protein pathways. • Iron homeostasis and metal transport systems were significantly disrupted. • Findings reveal microbial adaptation mechanisms to PFAS exposure.