Robert Quivey
| Title | Professor |
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| Institution | School of Medicine and Dentistry |
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| Department | Microbiology and Immunology in the Center for Oral Biology |
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| Address | University of Rochester Medical Center
School of Medicine and Dentistry
601 Elmwood Ave, Box 611
Rochester NY 14642
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| Title | Director |
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| Institution | University of Rochester Medical Center |
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| Department | Center for Oral Biology |
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| Phi Kappa Phi | |
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| Sigma Xi | |
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| Member- Pathogen Functional Genomics Research Advisory Committee | J. Craig Venter Institute and NIH | | 1996 |
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| 1999 | Chairman, Fellowships Committee | IADR/ AADR | | 2002 |
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| 2004 | President Elect, Microbiology and Immunology Research Group | IADR | | 2003 |
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| Graduate Alumni Award for Excellence in Graduate Education, University of Rochester Medical Center | | 2004 |
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| President, Microbiology & Immunology Research Group | IADR | | 2009 |
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| IADR Councilor for the Microbiology & Immunology Research Group | IADR |
Our research work is focused on a bacterium, Streptococcus mutans, which colonizes the human mouth from the time of tooth eruption until death. The persistence of the organism is remarkable and our efforts are directed to learning the biological means by which it chronically infects virtually every person in the developed nations. The infection requires two relatively simple-minded objectives: bind to tooth surfaces and then survive in the mouth. However, the mouth is a fairly inhospitable environment, containing between 400 and 500 competing bacterial species, volumes of saliva that are swallowed, desquamating soft tissue surfaces, and the swallowing of food (and adsorbed bacteria) as a bolus. Irreversible binding of tooth surfaces occurs by the action of extracellular enzymes produced by S. mutans, the glucosyltransferases (GTFs). These enzymes catalyze the conversion of sucrose, supplied in our diets, to long-chain, insoluble glucans that serve as the molecular scaffold for the formation of dental plaque. If not removed, physically from teeth, the growing mesh of glucan, food particles, bacteria, and salivary constituents continues to accumulate and forms a biofilm referred to as dental plaque. As plaque builds up, S. mutans becomes protected from the flushing effects of saliva and swallowing. In its protected niche, S. mutans metabolism of sugar results in the formation of organic acids and the rapid acidification of the surrounding milieu. As pH values plummet, several orders of magnitude in just seconds, S. mutans begins its adaptation to life at low pH values, where surrounding bacteria can not compete. Our work is in understanding the mechanisms of low pH adaptation and how it relates to bacterial virulence in biofilms.
Results from our efforts have shown that S. mutans utilizes a number of discrete mechanisms to survive acidic environments. Interestingly, we've found that some of the mechanisms are shared with other streptococcal pathogens, and some are shared with streptococcal and staphylococcal pathogens. For example, we've shown that the central acid-protective enzyme, the F-ATPase, is transcriptionally up-regulated ("on") at low pH, which is characteristic shared with S. pneumoniae (Kuhnert et al., 2004). Our data has also shown that S. mutans must make major alterations to its membrane to survive low pH, requiring the action of an enzyme called FabM, a condition that is apparently shared in Staphylococcus aureus (Fozo and Quivey, 2004). Further evidence from our group has shown that resistance to acid-stress overlaps stress from oxidative agents, such as hydrogen peroxide, and that control of oxygen metabolism by an enzyme called NADH oxidase is mediated, in part, by novel mechanisms unique to S. mutans (Karrupaiah et al., 2005). In all of this work, we have focused on identifying those elements that might be useful targets for therapeutic intervention. Our results have shown that identification of unique regulatory schemes or novel enzyme mechanisms involved in stress responses in S. mutans also have a possible usefulness in other human pathogens. We are pursuing or basic science goals, with the inclusion of translational work. For example, we are exploring the use of metal ions, with knowledge gained from DNA repair studies, to develop new therapies for bacterial infection (Faustoferri et al., 2005). We have also begun the use of transgenic mice to study early infection processes (Culp et al., 2005). And, finally, we are developing new technology, in conjunction with the Optics Institute, to rapidly determine the bacterial composition of clinical biofilm samples (Zhu et al., 2004).
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Gonzalez K, Faustoferri RC, Quivey RG. Role of DNA base excision repair in the mutability and virulence of Streptococcus mutans. Mol Microbiol. 2012 Jul; 85(2):361-77.
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Macgilvray ME, Lapek JD, Friedman AE, Quivey RG. Cardiolipin biosynthesis in Streptococcus mutans is regulated in response to external pH. Microbiology. 2012 Aug; 158(Pt 8):2133-43.
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Santiago B, Macgilvray M, Faustoferri RC, Quivey RG. The Branched-Chain Amino Acid Aminotransferase Encoded by ilvE Is Involved in Acid Tolerance in Streptococcus mutans. J Bacteriol. 2012 Apr; 194(8):2010-9.
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Derr AM, Faustoferri RC, Betzenhauser MJ, Gonzalez K, Marquis RE, Quivey RG. Mutation of the NADH Oxidase Gene (nox) Reveals an Overlap of the Oxygen- and Acid-Mediated Stress Responses in Streptococcus mutans. Appl Environ Microbiol. 2012 Feb; 78(4):1215-27.
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Beier BD, Quivey RG, Berger AJ. Identification of different bacterial species in biofilms using confocal Raman microscopy. J Biomed Opt. 2010 Nov-Dec; 15(6):066001.
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Sheng J, Baldeck JD, Nguyen PT, Quivey RG, Marquis RE. Alkali production associated with malolactic fermentation by oral streptococci and protection against acid, oxidative, or starvation damage. Can J Microbiol. 2010 Jul; 56(7):539-47.
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Kajfasz JK, Rivera-Ramos I, Abranches J, Martinez AR, Rosalen PL, Derr AM, Quivey RG, Lemos JA. Two Spx proteins modulate stress tolerance, survival, and virulence in Streptococcus mutans. J Bacteriol. 2010 May; 192(10):2546-56.
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Kajfasz JK, Martinez AR, Rivera-Ramos I, Abranches J, Koo H, Quivey RG, Lemos JA. Role of Clp proteins in expression of virulence properties of Streptococcus mutans. J Bacteriol. 2009 Apr; 191(7):2060-8.
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Zhu Q, Quivey RG, Berger AJ. Raman spectroscopic measurement of relative concentrations in mixtures of oral bacteria. Appl Spectrosc. 2007 Nov; 61(11):1233-7.
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Fozo EM, Scott-Anne K, Koo H, Quivey RG. Role of unsaturated fatty acid biosynthesis in virulence of Streptococcus mutans. Infect Immun. 2007 Mar; 75(3):1537-9.
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Koo H, Seils J, Abranches J, Burne RA, Bowen WH, Quivey RG. Influence of apigenin on gtf gene expression in Streptococcus mutans UA159. Antimicrob Agents Chemother. 2006 Feb; 50(2):542-6.
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Culp DJ, Quivey RQ, Bowen WH, Fallon MA, Pearson SK, Faustoferri R. A mouse caries model and evaluation of aqp5-/- knockout mice. Caries Res. 2005 Nov-Dec; 39(6):448-54.
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Faustoferri RC, Hahn K, Weiss K, Quivey RG. Smx nuclease is the major, low-pH-inducible apurinic/apyrimidinic endonuclease in Streptococcus mutans. J Bacteriol. 2005 Apr; 187(8):2705-14.
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Chatfield CH, Koo H, Quivey RG. The putative autolysin regulator LytR in Streptococcus mutans plays a role in cell division and is growth-phase regulated. Microbiology. 2005 Feb; 151(Pt 2):625-31.
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Kuhnert WL, Zheng G, Faustoferri RC, Quivey RG. The F-ATPase operon promoter of Streptococcus mutans is transcriptionally regulated in response to external pH. J Bacteriol. 2004 Dec; 186(24):8524-8.
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Zhu Q, Quivey RG, Berger AJ. Measurement of bacterial concentration fractions in polymicrobial mixtures by Raman microspectroscopy. J Biomed Opt. 2004 Nov-Dec; 9(6):1182-6.
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Fozo EM, Kajfasz JK, Quivey RG. Low pH-induced membrane fatty acid alterations in oral bacteria. FEMS Microbiol Lett. 2004 Sep 15; 238(2):291-5.
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Fozo EM, Quivey RG. The fabM gene product of Streptococcus mutans is responsible for the synthesis of monounsaturated fatty acids and is necessary for survival at low pH. J Bacteriol. 2004 Jul; 186(13):4152-8.
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Fozo EM, Quivey RG. Shifts in the membrane fatty acid profile of Streptococcus mutans enhance survival in acidic environments. Appl Environ Microbiol. 2004 Feb; 70(2):929-36.
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Kuhnert WL, Quivey Jr RG. Genetic and biochemical characterization of the F-ATPase operon from Streptococcus sanguis 10904. J Bacteriol. 2003 Mar; 185(5):1525-33.
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Bowen WH, Quivey RG, Smith AV. Glucosyltransferase inactivation reduces dental caries. J Dent Res. 2001 Jun; 80(6):1505-6.
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Quivey RG, Kuhnert WL, Hahn K. Genetics of acid adaptation in oral streptococci. Crit Rev Oral Biol Med. 2001; 12(4):301-14.
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Quivey RG, Faustoferri R, Monahan K, Marquis R. Shifts in membrane fatty acid profiles associated with acid adaptation of Streptococcus mutans. FEMS Microbiol Lett. 2000 Aug 1; 189(1):89-92.
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Quivey RG, Kuhnert WL, Hahn K. Adaptation of oral streptococci to low pH. Adv Microb Physiol. 2000; 42:239-74.
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Hahn K, Faustoferri RC, Quivey RG. Induction of an AP endonuclease activity in Streptococcus mutans during growth at low pH. Mol Microbiol. 1999 Mar; 31(5):1489-98.
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Burne RA, Quivey RG, Marquis RE. Physiologic homeostasis and stress responses in oral biofilms. Methods Enzymol. 1999; 310:441-60.
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Smith AJ, Quivey RG, Faustoferri RC. Cloning and nucleotide sequence analysis of the Streptococcus mutans membrane-bound, proton-translocating ATPase operon. Gene. 1996 Dec 12; 183(1-2):87-96.
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Vacca-Smith AM, Venkitaraman AR, Quivey RG, Bowen WH. Interactions of streptococcal glucosyltransferases with alpha-amylase and starch on the surface of saliva-coated hydroxyapatite. Arch Oral Biol. 1996 Mar; 41(3):291-8.
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Quivey RG, Faustoferri RC, Clancy KA, Marquis RE. Acid adaptation in Streptococcus mutans UA159 alleviates sensitization to environmental stress due to RecA deficiency. FEMS Microbiol Lett. 1995 Mar 1; 126(3):257-61.
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Quivey RG, Faustoferri RC, Reyes SD. UV-resistance of acid-adapted Streptococcus mutans. Dev Biol Stand. 1995; 85:393-8.
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Burne RA, Quivey RG. Use of transposons to dissect pathogenic strategies of gram-positive bacteria. Methods Enzymol. 1994; 235:405-26.
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Quivey RG, Kriger PS. Raffinose-induced mutanase production from Trichoderma harzianum. FEMS Microbiol Lett. 1993 Sep 15; 112(3):307-12.
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Quivey RG, Faustoferri RC. In vivo inactivation of the Streptococcus mutans recA gene mediated by PCR amplification and cloning of a recA DNA fragment. Gene. 1992 Jul 1; 116(1):35-42.
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Quivey RG, Faustoferri RC, Belli WA, Flores JS. Polymerase chain reaction amplification, cloning, sequence determination and homologies of streptococcal ATPase-encoding DNAs. Gene. 1991 Jan 2; 97(1):63-8.
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Quivey RG, Bowen WH. A computer program designed for the analysis of data from rat caries studies. Caries Res. 1991; 25(3):191-6.
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Falcone DL, Quivey RG, Tabita FR. Transposon mutagenesis and physiological analysis of strains containing inactivated form I and form II ribulose bisphosphate carboxylase/oxygenase genes in Rhodobacter sphaeroides. J Bacteriol. 1988 Jan; 170(1):5-11.
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Quivey RG. The use of DNA probes in dental diagnosis and therapy. Adv Dent Res. 1987 Oct; 1(1):99-108.
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Quivey RG, Tabita FR. Cloning and expression in Escherichia coli of the form II ribulose 1,5-bisphosphate carboxylase/oxygenase gene from Rhodopseudomonas sphaeroides. Gene. 1984 Nov; 31(1-3):91-101.
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