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 Fe3+ is deposited and, when necessary, mobilized as Fe2+ for metabolic requirements. In Pseudomonas aeruginosa, Fe3+ is compartmentalized in bacterioferritin (BfrB), and its mobilization as Fe2+ requires specific binding of a ferredoxin (Bfd) to reduce the stored Fe3+. 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 P. aeruginosa 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.

中文翻译：

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抑制铜绿假单胞菌中细菌铁蛋白的铁动员会破坏生物膜的形成，而与环境中铁的可用性无关。

尽管铁是细菌必不可少的，但营养素却存在毒性和溶解性问题。细菌借助铁存储蛋白来解决这些问题，铁蛋白会沉积Fe3 +，并在必要时动员为代谢所需的Fe2 +。在铜绿假单胞菌中，Fe3 +在细菌铁蛋白（BfrB）中区分开，并且其作为Fe2 +的动员需要铁氧还蛋白（Bfd）的特异性结合以减少储存的Fe3 +。阻断BfrB-Bfd复合物会导致BfrB中不可逆的铁积累和胞质铁剥夺。因此，考虑到生物膜发育所需的细胞内铁充足性，我们假设阻断铜绿假单胞菌中的BfrB-Bfd相互作用会损害生物膜发育。我们的结果表明，即使在铁充足的培养条件下，BfrB-Bfd复合物被阻滞的浮游生物和生物膜包埋的细胞也表现出胞质铁缺乏和生物膜发育不良。这些结果强调了对BfrB-Bfd复合物的抑制，这是失调铁稳态并可能控制生物膜的合理靶点。