Journal article
PhoPR Contributes to Staphylococcus aureus Growth during Phosphate Starvation and Pathogenesis in an Environment-Specific Manner
Infection and immunity, Vol.86(10), e00371-18
10/01/2018
DOI: 10.1128/IAI.00371-18
PMCID: PMC6204748
PMID: 30061377
Abstract
Microbial pathogens must obtain all essential nutrients, including phosphate, from the host. To optimize phosphate acquisition in diverse and dynamic environments, such as mammalian tissues, many bacteria use the PhoPR two-component system.
Microbial pathogens must obtain all essential nutrients, including phosphate, from the host. To optimize phosphate acquisition in diverse and dynamic environments, such as mammalian tissues, many bacteria use the PhoPR two-component system. Despite the necessity of this system for virulence in several species, PhoPR has not been studied in the major human pathogen
Staphylococcus aureus
. To illuminate its role in staphylococcal physiology, we initially assessed whether PhoPR controls the expression of the three inorganic phosphate (P
i
) importers (PstSCAB, NptA, and PitA) in
S. aureus
. This analysis revealed that PhoPR is required for the expression of
pstSCAB
and
nptA
and can modulate
pitA
expression. Consistent with a role in phosphate homeostasis, PhoPR-mediated regulation of the transporters is influenced by phosphate availability. Further investigations revealed that PhoPR is necessary for growth under P
i
-limiting conditions, and in some environments, its primary role is to induce the expression of
pstSCAB
or
nptA
. Interestingly, in other environments, PhoPR is necessary for growth independent of P
i
transporter expression, indicating that additional PhoPR-regulated factors promote
S. aureus
adaptation to low-P
i
conditions. Together, these data suggest that PhoPR differentially contributes to growth in an environment-specific manner. In a systemic infection model, a mutant of
S. aureus
lacking PhoPR is highly attenuated. Further investigation revealed that PhoPR-regulated factors, in addition to P
i
transporters, are critical for staphylococcal pathogenesis. Cumulatively, these findings point to an important role for PhoPR in orchestrating P
i
acquisition as well as transporter-independent mechanisms that contribute to
S. aureus
virulence.
Details
- Title: Subtitle
- PhoPR Contributes to Staphylococcus aureus Growth during Phosphate Starvation and Pathogenesis in an Environment-Specific Manner
- Creators
- Jessica L. Kelliher - University of Illinois Urbana-ChampaignJana N. Radin - University of Illinois Urbana-ChampaignThomas E. Kehl-Fie - University of Illinois Urbana-Champaign
- Resource Type
- Journal article
- Publication Details
- Infection and immunity, Vol.86(10), e00371-18
- Publisher
- American Society for Microbiology
- DOI
- 10.1128/IAI.00371-18
- PMID
- 30061377
- PMCID
- PMC6204748
- ISSN
- 0019-9567
- eISSN
- 1098-5522
- Grant note
- ; R01 AI118880 / ; 5-FY15-30 / ; K22 AI104805 / ;
- Alternative title
- S. aureus PhoPR and Virulence
- Language
- English
- Date published
- 10/01/2018
- Academic Unit
- Microbiology and Immunology
- Record Identifier
- 9984618638802771
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