Arsenic resistance in fungi conferred by extracellular bonding and vacuole-septa compartmentalization.

• Extracellular bonding and intracellular detainment confer As resistance of fungi. • Fungal cell wall contributed average 80 % of the total immobilized As by fungi. • The vacuole As accounted for average 55 % of the protoplast As in fungal cells. • Fungal septa is newly found to compartmentise or immobilize As. • GSH content is a reasonable indicator for As tolerance in fungal protoplast. Microbes play a crucial role in arsenic (As) biogeochemical cycling and show great potential for environmental detoxification and bioremediation. Efflux, transformation, and compartmentalization are key processes in microbial As resistance. However, organelle specific As detoxification and fate during intracellular transfer and compartmentalization is not well understood. We conducted a time course experiment (2–5 days) of the organelle separation for fungal strains to explore subcellular As distributions. After exposure to 10 mg L−1 of arsenate (As(V)), the As accumulation among fungal organelles was generally in the order of extracellular (65 %) > cell wall (15 %) > vacuole (10 %) > other organelles (8 %). The vacuole As accounted for 55 % of the protoplast As. Extracellular bonding and vacuole compartmentalization were the main mechanisms of As resistance in the fungal strains tested. Glutathione (GSH) increases in fungal protoplast in response to As toxicity, acting as a reasonable indicator of As tolerance. Fourier transform infrared (FT-IR) spectroscopy indicated that carboxyl and amines groups within fungal cell walls potentially bind with As preventing As influx. Further analysis using scanning transmission X-ray microscopy (STXM) identified that fungal septa besides vacuole could also immobilize As. [ABSTRACT FROM AUTHOR]