10.1021/acsinfecdis.9b00398.s001 Anabel Soldano Anabel Soldano Huili Yao Huili Yao Josephine R. Chandler Josephine R. Chandler Mario Rivera Mario Rivera Inhibiting Iron Mobilization from Bacterioferritin in <i>Pseudomonas aeruginosa</i> Impairs Biofilm Formation Irrespective of Environmental Iron Availability American Chemical Society 2020 dysregulate iron homeostasis biofilm development iron storage proteins Fe cytosolic iron deprivation BfrB-Bfd Pseudomonas aeruginosa Impairs Biofilm Formation Irrespective Environmental Iron Availability iron-sufficient culture conditions Inhibiting Iron Mobilization exhibit cytosolic iron deficiency intracellular iron sufficiency requirement 2020-01-15 13:03:46 Journal contribution https://acs.figshare.com/articles/journal_contribution/Inhibiting_Iron_Mobilization_from_Bacterioferritin_in_i_Pseudomonas_aeruginosa_i_Impairs_Biofilm_Formation_Irrespective_of_Environmental_Iron_Availability/11618361 Although iron is essential for bacteria, the nutrient presents problems of toxicity and solubility. Bacteria circumvent these problems with the aid of iron storage proteins where Fe<sup>3+</sup> is deposited and, when necessary, mobilized as Fe<sup>2+</sup> for metabolic requirements. In <i>Pseudomonas aeruginosa</i>, Fe<sup>3+</sup> is compartmentalized in bacterioferritin (BfrB), and its mobilization as Fe<sup>2+</sup> requires specific binding of a ferredoxin (Bfd) to reduce the stored Fe<sup>3+</sup>. Blocking the BfrB-Bfd complex leads to irreversible iron accumulation in BfrB and cytosolic iron deprivation. Consequently, given the intracellular iron sufficiency requirement for biofilm development, we hypothesized that blocking the BfrB-Bfd interaction in <i>P. aeruginosa</i> would impair biofilm development. Our results show that planktonic and biofilm-embedded cells where the BfrB-Bfd complex is blocked exhibit cytosolic iron deficiency, and poorly developed biofilms, even in iron-sufficient culture conditions. These results underscore inhibition of the BfrB-Bfd complex as a rational target to dysregulate iron homeostasis and possibly control biofilms.