Iron (Fe) is a trace nutrient required by nearly all organisms, thus the importance of Fe homeostasis in bacteria. Jeff Boyd’s Lab, Dept. of Biochemistry & Microbiology at Rutgers demonstrates how Fpa interacts with Fur to alleviate its repression during iron limitation, enabling the transcription of iron uptake genes in Staphylococcus aureus:
- Fpa is essential for growth of S. aureus under iron-limiting conditions, and this essentiality is bypassed by mutations that inactivate the iron-responsive transcriptional regulator Fur.
- Fpa binds to Fur and decreases Fur's DNA-binding ability, suggesting Fpa functions to alleviate Fur-dependent repression under iron limitation.
- Fpa binds iron(II) in vitro, consistent with a role in iron homeostasis.
Boyd JM, Ryan Kaler K, Esquilín-Lebrón K, Pall A, Campbell CJ, Foley ME, Rios-Delgado G, Mustor EM, Stephens TG, Bovermann H, Greco TM, Cristea IM, Carabetta VJ, Beavers WN, Bhattacharya D, Skaar EP, Shaw LN, Stemmler TL. 2024. Fpa (YlaN) is an iron(II) binding protein that functions to relieve Fur-mediated repression of gene expression in Staphylococcus aureus. mBio 15:e02310-24.
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