Bacillithiol has a role in Fe-S cluster biogenesis in Staphylococcus aureus
Zuelay Rosario-Cruz1, Harsimranjit K Chahal1, Laura A Mike2
1Department of Biochemistry and Microbiology, Rutgers University, New Brunswick, NJ, 08901, USA.
Molecular Microbiology
|July 3, 2015
Summary
Bacillibactin (BSH), a thiol produced by Staphylococcus aureus, is crucial for iron homeostasis and iron-sulfur (Fe-S) cluster transport. Lacking BSH causes growth defects and impaired Fe-S cluster enzyme activity.
Area of Science:
- Microbiology
- Biochemistry
- Molecular Biology
Background:
- Staphylococcus aureus produces bacillibactin (BSH), a low-molecular-weight (LMW) thiol, but not glutathione.
- The specific metabolic roles of BSH in S. aureus remain incompletely understood.
Purpose of the Study:
- To investigate the function of BSH in S. aureus metabolism.
- To elucidate the involvement of BSH in iron homeostasis and iron-sulfur (Fe-S) cluster biogenesis.
Main Methods:
- Construction and phenotypic analysis of BSH-deficient S. aureus strains.
- Assay of Fe-S cluster-dependent enzyme activities (LeuCD, IlvD, aconitase, glutamate synthase).
- Investigation of Fe-S cluster carrier protein interactions (Nfu, SufA).
Main Results:
- BSH-deficient strains exhibited growth defects under aerobic and anaerobic conditions, alleviated by iron or specific amino acids.
- Decreased activities of Fe-S cluster-dependent enzymes and impaired Fe-S cluster biogenesis were observed in BSH-deficient cells.
- Functional overlap between BSH and Fe-S cluster carriers (Nfu, SufA) was identified, with SufA confirmed as an Fe-S cluster carrier.
Conclusions:
- BSH plays a significant role in maintaining iron homeostasis in S. aureus.
- BSH is involved in the transport of Fe-S clusters to apo-proteins, potentially acting in concert with Fe-S carrier proteins like SufA.
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