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.