Microbially induced corrosion (MIC) costs trillions of dollars yearly by damaging metal infrastructure. MIC occurs when microorganisms oxidize solid elemental metals using redox-active metabolites such as phenazines, which create soluble metal ions. Phenazine-mediated corrosion has been well studied for iron. Whether such pathways can solubilize the economically critical metal cobalt through thermodynamically favourable reactions remains unknown. We hypothesized that Co(0) corrosion by the model bacterium Pseudomonas chlororaphis subspecies aureofaciens depends on phenazine availability. To test this hypothesis, we compared the corrosion of Co(0) wires and phenazine production over one-week incubations with either wild-type cells or a deletion mutant devoid of the phz operon incapable of phenazine biosynthesis. All experiments with live cells were compared to abiotic controls with spent medium, phenazine standards, and sterile medium. Soluble Co(2+) concentrations measured with ICP-MS showed that live cells were essential to cobalt corrosion. The wild-type and {Delta}phz mutant corroded 30-40% of the wire mass [equivalent to ~ 2,500 M soluble Co(2+)], which was at least 3-fold higher than mass losses for abiotic controls. Both strains decreased wire diameters and produced considerable pitting compared to abiotic controls imaged with SEM-EDX. Cobalt corrosion could be slowed through Co(2+) toxicity and cobalt oxide precipitation. These findings counter studies with iron and biosynthetic gene cluster analyses suggest that corrosion occurred through alternative mechanisms that rely on metal-binding ligand production. This work expands the repertoire of metals solubilized by MIC and shows that MIC can be used for critical metal recovery at the lab scale.