Pseudomonas aeruginosa displays remarkable adaptability in chronic infections by exploiting heme as its primary iron source at the expense of siderophore uptake. Previous studies have identified a pivotal role for the heme metabolites BVIX β/δ in the regulation of Type IV pili-dependent motility and biofilm formation. Thus, the heme metabolites integrate the switch in iron source with lifestyle adaptations required for chronic infection. The mechanism by which the BVIX metabolites directly or indirectly regulate such lifestyle adaptations remains elusive. In this study, through a combination of thermal proteome profiling (TPP) followed by quantitative mass spectrometry (MS), we identified a BVIX-binding protein PA5271 encoded in a three-gene operon (pa5269-pa-5270-pa5271). PA5271 is annotated as a helix-turn-helix DNA-binding protein and purifies as a dimer that binds BVIX but not BVIX or BVIX. Deletion of the gene renamed bdrB (biliverdin-dependent regulator responsive to BVIX) displayed a marked reduction in Type IV pili (TFP) associated motilities including twitching.