Summary of study ST000247

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR000199. The data can be accessed directly via it's Project DOI: 10.21228/M8P304 This work is supported by NIH grant, U2C- DK119886.

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Study IDST000247
Study TitleDetermining the metabolic profile of wildtype and nos mutant Staphylococcus aureus grown in media lacking glucose using targeted LC/MS
Study TypeSingle time point
Study SummaryWhole cells from wildtype, nos mutant, SrrAB mutant, SrrAB nos double mutant, and complement strains will be isolated for targeted metabolite analysis. In parallel, supernatants (extracellular metabolites) will also be analyzed for their metabolic profile.
Institute
University of Florida
DepartmentSECIM
Last NameRice
First NameKelly
Emailkcrice@ufl.edu
Submit Date2015-02-17
Num Groups7
Total Subjects21
Analysis Type DetailLC-MS
Release Date2019-01-22
Release Version1
Kelly Rice Kelly Rice
https://dx.doi.org/10.21228/M8P304
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR000199
Project DOI:doi: 10.21228/M8P304
Project Title:Utilization of a global and targeted metabolomics approach to probe the effects of nitric oxide on physiology of the pathogen Staphylococcus aureus
Project Type:Targeted LCMS Metabolomics
Project Summary:Staphylococcus aureus is a significant cause of morbidity and mortality in both hospital settings and the community at-large, and methicillin-resistant S. aureus (MRSA) has been recently categorized by the CDC as a significant antibiotic-resistant threat. As such, there exists an on-going critical need to study S. aureus genes that promote growth and resistance to host immune responses, so that their encoded products can eventually be evaluated for potential as novel antimicrobial targets. In this respect, S. aureus nitric-oxide (NO) synthase (saNOS) and NO-reductase (saNOR) have been recently shown to dramatically affect the physiology of this pathogen. Specifically, nos mutants have displayed decreased virulence in both subcutaneous abscess and sepsis models of infection, and our own research has suggested that NO produced via saNOS has a negative effect on endogenous reactive oxygen species (ROS) accumulation under growth conditions promoting aerobic respiration and may regulate metabolism in an as-yet unknown fashion. Our research has also demonstrated a role for saNOR in modulating cellular NO levels when exposed to exogenous NO donor and may contribute to cellular metabolism under conditions of nitrosative stress. Therefore, overall hypothesis of this proposal is that modulation of exogenous and endogenous NO levels (by saNOR and saNOS, respectively) represent novel metabolic adaptations that contribute to S. aureus survival during infection. To this end, a global untargeted metabolomics approach will be employed to complete two research aims: Aim 1: Compare the effect of saNOR on S. aureus metabolism when grown in the presence and absence of exogenous NO. Aim 2: Identify the effects of endogenous NO produced by saNOS on S. aureus metabolism when grown under conditions promoting aerobic respiration. These proposed studies will help catalogue the exact metabolic changes that occur as a function of saNOS and saNOR, which will help unravel the upstream regulatory circuits and downstream cellular targets of both of these enzymes.
Institute:University of Florida
Department:Microbiology and Cell Science
Laboratory:Kelly Rice
Last Name:Rice
First Name:Kelly
Address:Room 1130, 1355 Museum Dr, UF campus, 32611-0700
Email:kcrice@ufl.edu
Phone:352-392-1192
Funding Source:Southeastern Center for Integrated Metabolomics (SECIM) pilot and feasibility funding, NIH U24 DK097209
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