Project description:This study addresses the impact of zinc limitation on the opportunistic human pathogen, Pseudomonas aeruginosa. Zinc limitation was assessed in the P. aeruginosa PAO1 strain using an isogenic deletion mutant lacking the periplasmic, zinc solute-binding protein, znuA (PA5498). ZnuA delivers bound zinc to its cognate ABC transporter, ZnuBC, for import into the cytoplasm. Our transcriptional analyses revealed P. aeruginosa to possess a multitude of zinc acquisition mechanisms, each of which were highly up-regulated in the zinc-deficient znuA mutant strain. P. aeruginosa also utilized zinc-independent paralogues of zinc-dependent genes to maintain cellular function under zinc limitation. Together, these data reveal the complex transcriptional response and versatility of P. aeruginosa to zinc depletion.