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Supported by an IDeA grant from the National Center
for Research Resources, NIH
BS Bates College 1970 biology
MA SUNY Buffalo 1978 microbiology
PhD SUNY Buffalo 1989 oral biologyProfessor Baker’s laboratory is involved in research on periodontal disease. She has developed a mouse model in which oral infection with the human periodontopathic microorganism, Porphyromonas gingivalis, results in loss of alveolar bone. Using this model and strains of genetically immunocompetent or immunodeficient mice, she and her colleagues are investigating the role of the host immune system in bone loss. It appears that an intact immune system, rather than being protective, is actively involved in the induction of bone loss. She is also using this model to test various chemical agents as preventatives for bone loss. Most recently, Professor Baker and her colleagues have established that susceptibility to bone loss after infection has a genetic component. They are investigating the possible loci involved. Professor Baker’s laboratory is also involved in investigations on the effects of subinhibitory concentrations of antibiotics on microbial protein expression. Changes in protein expression sometimes lead to changes in the ability of the host immune system to clear the bacteria.
Baker, P.J., M. Dixon, R.T. Evans, and D.C. Roopenian. 2000. Heterogeneity of Porphyromonas gingivalis strains in the induction of alveolar bone loss in mice. Oral Microbiology and Immunology 15: 27-32.
Baker, P.J., H.A. Rotch, L. Trombelli, and U.M.E. Wikesjo. 2000. An in vitro screening method to evaluate root conditioning protocols for periodontal regenerative procedures. J. Periodontol. 71: 1139-1143.
Baker, P.J., L. DuFour, M. Dixon, and D.C. Roopenian. 2000. Adhesion molecule deficiencies increase Porphyromonas gingivalis-induced alveolar bone loss in mice. Infection and Immunity. 68: 3103-3108.
Baker. P.J., M. Dixon, and D.C. Roopenian. 2000. Genetic control of susceptibility to alveolar bone loss in mice. Infection and Immunity 68: 5864-5868.
Baker, P.J. 2000. The Role of Immune Responses in Bone Loss During Periodontal Disease. Microbes and Infection 2: 1181-1192.
BA St. Mary’s College of MD, 1995, Biology
PhD University of Montana, 2000, Organismal Biology
Dr. Bavis’ research focuses on the control of breathing and, in particular, how the environment alters breathing in early life and adulthood (i.e. phenotypic plasticity). He is also very interested in the physiological ecology of burrowing birds and mammals.Bavis, RW, Johnson, RA, Ording, KM, Otis, JP & Mitchell, GS. (2006) Respiratory plasticity after perinatal hypercapnia in rats. Respir. Physiol. Neurobiol. 153:78-91.
Bavis, RW, Russell, KER, Simons, JC & Otis, JP. (2007) Hypoxic ventilatory responses in rats after hypercapnic hyperoxia and intermittent hyperoxia. Respir. Physiol. Neurobiol. 155:193-202.
Bavis, RW, Powell, FL, Bradford, A, Hsia, CCW, Peltonen, JE, Soliz, J, Zeis, B, et al. (2007) Respiratory plasticity in response to changes in oxygen supply and demand. Integr. Comp. Biol. 47: 532-551.
Bavis, RW & Mitchell, GS. (2008) Long-term effects of the perinatal environment on respiratory control. J. Appl. Physiol. 104: 1220-1229.
Bavis, RW, Wenninger, JM, Miller BM, Fergusson, EK, Olson, EB Jr., Mitchell, GS & Bisgard, GE. (2008) Respiratory plasticity after perinatal hyperoxia is not prevented by antioxidant supplementation. Respir. Physiol. Neurobiol. 160:301-312.
Doperalski, NJ, Sandhu, MS, Bavis, RW, Reier, PJ & Fuller, DD. Sex differences in respiratory recovery following high cervical spinal hemisection in rats. Respir. Physiol. Neurobiol., in press.
Kilgore, DL, Jr., Boggs, DF, Kilgore, TJ, Colby, C, Williams, BR, Jr. & Bavis, RW. Ventilatory and metabolic responses of burrowing owls, Athene cunicularia, to moderate and extreme hypoxia: analysis of the hypoxic ventilatory threshold vs. hemoglobin oxygen affinity relationship in birds. Comp. Physiol. Biochem. A, in press.
BA, Anderson College, 1978
PhD, Purdue University, 1984Professor Lawson is investigating the rapid and selective turnover of viral enzymes known as the 3C proteases, which are responsible for most of the processing of picornavirus polyproteins generated during infections of mammalian cells. His research group has shown that the 3C protease of the encephalomyocarditis virus (EMCV) and hepatitis A virus (HAV) are rapidly degraded by the ubiquitin/26S proteasome system. Recently, his lab has mapped and characterized ten-amino acid long regions in these proteins that are required for their recognition by the ubiquitin/26S proteasome system. His current research includes: 1) a kinetic examination of the mechanism by which a particular ubiquitin-protein ligase selectively associates with the 3C protease proteins and catalyzes ubiquitin conjugation; 2) the development of an inducible in vivo expression system that will allow explorations of the role the destruction of the 3C proteases plays in picornavirus replication; and 3) studies of how processing of the HAV polyprotein and the susceptability of HAV 3C protease toward ubiquitin-dependent degradation are linked.
Lam, Y. A., Lawson, T. G., Velayutham, M., Zweier, J., and Pickart, C. M. (2002) ATPase Subunit of the 26S Proteasome Recognizes Polyubiquitin Chains. Nature 416, 763-767.Lawson, T. G., Sweep, M. E., Schlax, P. E., Bohnsack, R. N., and Haas, A. L. (2001) Kinetic Analysis of the Conjugation of Ubiquitin to Picornavirus 3C Proteases Catalyzed by the Mammalian Ubiquitin-Protein Ligase E3". J. Biol. Chem. 276, 39629-39637
Lawson, T. G., Gronros, D. L., Evans, P. E., Bastien, M. C., Michalewich, K. M., Clark, J. K., Edmonds, J. H., Graber, K. H., Werner, J. A., Lurvey, B. A., and Cate, J. M. (1999) Identification and Characterization of a Protein Destruction Signal in the Encephalomyocarditis Virus 3C Protease. J. Biol. Chem. 274, 9871-9880.
Gladding, R. L., Haas, A. L., Gronros, D. L., and Lawson, T. G. (1997) Evaluation of the Susceptibility of the 3C Proteases of Hepatitis A Virus and Poliovirus to Degradation by the Ubiquitin-mediated Proteolytic System. Biochem. Biophys. Res. Commun. 238, 119 -125.
Rebecca Sommer, Ph.D
Associate Professor of Biology and Environmental Sciences
Bates College
rsommer@bates.edu
http://www.bates.edu/x57609.xml
BS, University of Wisconsin - Madison, 1992, Pharmacology & Toxicology
PhD, University of Wisconsin - Madison, 1998, PharmacologyTCDD, or dioxin, belongs to a family of structurally similar chemicals which include some polychlorinated biphenyls (PCBs). Significant amounts of these chemicals have entered the environment as contaminants and/or industrial products. The Sommer laboratory investigates the role that beta-adrenergic receptor (β-AR) signaling plays in dioxin-induced cardiovascular toxicity. β-ARs and their signal transduction systems give the normal heart the ability to increase its output by several-fold within a matter of seconds following activation by catecholamines. β-AR signaling also plays an important role in the processes of heart failure. The Laboratory’s work demonstrates that developmental exposure to relatively low doses of dioxin reduces β-AR responsiveness, most likely by altering β-AR signal transduction upstream of adenylyl cyclase. It is possible that TCDD directly alters transcriptional expression of β-AR genes.
Sommer, R.J., and Peterson, R.E. (1997). In utero and lactational exposure of the mouse to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD): Effects on male reproductive tract development. Dioxin ‘97, Organohalogen Compounds 34, 360-363.
Flaws, J.A., Sommer, R.J., Silbergeld, E., Peterson, R.E.,and Hirshfield, A.N. (1997). In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces genital dysmorphogenesis in the female rat. Toxicol. Appl. Pharmacol. 147, 351-362.
Sommer, R.J., Sojka, K.M., Pollenz, R.S., Cooke, P.S., and Peterson, R.E. (1999). Ah receptor and ARNT protein and mRNA concentrations in rat prostate: Effects of age and 2,3,7,8-tetrachlorodibenzo-p-dioxin. Toxicol. Appl. Pharmacol. 155, 177-189.
Dienhart, M.K., Sommer, R.J., Silbergeld, E., Peterson, R.E., and Hirshfield, A.N. (2000). Gestational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin induces developmental defects in the rat vagina. Toxicol. Sci. 56(1), 141-149.
Lewis, B.C., Hudgins, S., Lewis, A., Schorr, K., Sommer, R.J., Peterson, R.E., Flaws, J.A., and Furth, P.A. (2001). In utero and lactational treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin impairs mammary gland differentiation but does not block the response to exogenous estrogen in the post pubertal female rat. Toxicol. Sci. 62, 46-53.
Sommer, R.J. (2004). A Successful AREA Grant Proposal in the Biological Sciences. Council on Undergraduate Research Quarterly, 24(3), 125-128.
Sommer, R.J., Hume, A.J., Ciak, J.M., VanNostrand, J.J., Friggens, M. and Walker, M.K. (2005). Early developmental 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure decreases chick embryo heart chronotropic response to isoproterenol but not to agents affecting signals downstream of the beta-adrenergic receptor. Toxicol. Sci. 83, 363-371.