Greg Somerville

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Greg Somerville

Professor School of Veterinary Medicine and Biomedical Sciences University of Nebraska-Lincoln

Contact

Address
VBS 155
Lincoln NE 68583-0905
Phone
402-472-6063 On-campus 2-6063
Email
gsomerville3@unl.edu

Greg Somerville's chief research focus is the elucidation of mechanisms by which bacteria control virulence factor expression in response to nutrient availability. Specifically, his interest is in the function of central metabolism in regulating pathogenesis.

A professor in the School of Veterinary Medicine and Biomedical Sciences at the University of Nebraska–Lincoln, he is also affiliated with the UNL's Department of Biochemistry and the Redox Biology Center. Dr. Somerville earned a doctorate in Biology from the University of Texas at Dallas under the supervision of Larry Reitzer. Prior to joining Nebraska, he was a postdoctoral research fellow in the Laboratory of Human Bacterial Pathogenesis at the Rocky Mountain Laboratories in Hamilton, MT.

Education

  • Ph.D. in Bacterial Physiology, University of Texas at Dallas, 1999
  • M.S. in Molecular Biology, University of Texas at Dallas, 1993
  • B.S. in Molecular Biology, University of Texas at Dallas, 1988

Publications

Complete List of Published Work in MyBibliography: 

  1. Somerville, G., C.A. Mikoryak, and L. Reitzer, Physiological characterization of Pseudomonas aeruginosa during exotoxin A synthesis: glutamate, iron limitation, and aconitase activity. J Bacteriol, 1999. 181:1072-1078. PMCID: PMC93482. 
  2. Somerville, G.A., et al., Staphylococcus aureus aconitase inactivation unexpectedly inhibits post-exponential-phase growth and enhances stationary-phase survival. Infect Immun, 2002. 70:6373-6382. PMCID: PMC130419.
  3. Somerville, G.A., et al., Synthesis and deformylation of Staphylococcus aureus delta-toxin are linked to tricarboxylic acid cycle activity. J Bacteriol, 2003. 185:6686-6694. PMCID: PMC262117.
  4. Somerville, G.A., et al., Correlation of acetate catabolism and growth yield in Staphylococcus aureus: Implications for host-pathogen interactions. Infect Immun, 2003. 71:4724-4732. PMCID: PMC166023.
  5. Sadykov, M.R., et al., Tricarboxylic acid cycle-dependent regulation of Staphylococcus epidermidis polysaccharide intercellular adhesin synthesis. J Bacteriol, 2008. 190:7621-7632. PMCID: PMC2583607.
  6. Sadykov, M.R., et al., Using NMR metabolomics to investigate tricarboxylic acid cycle dependent signal transduction in Staphylococcus epidermidis. J. Biol. Chem., 2010. 285:36616–36624. PMCID: PMC2978590.
  7. Vuong, C., et al., Staphylococcus epidermidis polysaccharide intercellular adhesin production significantly increases during tricarboxylic acid cycle stress. J Bacteriol, 2005. 187:2967-2973. PMCID: PMC1082835.
  8. Gaupp, R., et al., RpiRc Is a Pleiotropic Effector of Virulence Determinant Synthesis and Attenuates Pathogenicity in Staphylococcus aureus. Infect Immun, 2016. 84:2031-2041. PMCID: PMC4936357.
  9. Gardner S.G., et al., Metabolic mitigation of Staphylococcus aureus vancomycin intermediate-level susceptibility. Antimicrob Agents Chemother. 2018. 62:e01608-17. PMCID: PMC5740343
  10. Gaupp, R., et al., Staphylococcus aureus metabolic adaptations during the transition from a daptomycin susceptible phenotype to a daptomycin non-susceptible phenotype. Antimicrob Agents Chemother, 2015. 59:4226-4238. PMCID: PMC4468685.
  11. Stark, J.L., et al., Identification of low-molecular-weight compounds inhibiting growth of corynebacteria: potential lead compounds for antibiotics. ChemMedChem, 2014. 9:282-285. PMCID: PMC3977743.
  12. Zhu, Y., et al., Tricarboxylic acid cycle-dependent attenuation of Staphylococcus aureus in vivo virulence by selective inhibition of amino acid transport. Infect Immun, 2009. 77:4256-4264. PMCID: PMC2747957.

Grants

  • NIAID/NIH. 1R01AI14816
    PI Robert Gennis (University of Illinois Urbana-Champaign)
    2021-2025
    Metabolomics of Staphylococcal Respiration
    Role: Co-investigator
  • Zoetis Inc.
    Somerville (PI)
    07/01/2015-06/30/2022
    “Fermentation media formulation and optimization”
    The objective of this contract is to provide metabolic advice on the optimization of fermentation processes. This work encompasses many bacterial species.
    Role: Principal investigator