Biomedical Sciences Department |
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| Aaron Baxter,
Ph.D.
Assistant Professor Biomedical Sciences Department 313 Henry Hall Allendale, Michigan 49401 Phone: 616-331-2888 Fax: 616-331-2090 email: baxteraa@gvsu.edu |
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FALL OFFICE HOURS: |
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| COURSES TAUGHT BMS 212 - Intro Microbiology BMS 213 - Microbiology Laboratory BMS 412 - Medical Bacteriology BMS 413 - Medical Bacteriology Laboratory |
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EDUCATION/TRAINING |
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| RESEARCH INTERESTS Much of what occurs in science revolves around doing research. Research answers the questions of how something works often leading to applications that help our world. Examples showing either the eradication and/or control of many devastating diseases illustrate how an understanding of the mechanisms of pathogenesis leads to ways of fighting a disease. My research has revolved around understanding the pathogenic mechanisms of Salmonella. The genes involved in Salmonella pathogenesis are found in specific areas known as pathogenicity islands. These islands contain a large number of genes involved in the formation of the type III secretion system which is vital for bacterial invasion of intestinal cells to occur. The focus for my research has been on the regulatory genes that control activation and repression of the invasion genes. These efforts identified a repressor known as hilE. I began my analysis by mapping the hilE regulator, to the chromosomes of serovar Typhimurium and serovar Typhi. My efforts placed the hilE gene at centisome 98. Analysis of this region revealed a ~40 kb region that was specific to Salmonella serovars. This region on closer inspection had many of the characteristics seen in the other pathogenicity islands found in Salmonella. The only other gene that has been identified in this region of the Salmonella genome is the iicA gene, (induced intracellularly A gene), a gene shown to be induced upon Salmonella internalization into host cells. This evidence led to identifying this region of the Salmonella genome as Salmonella Pathogenicity Island 6 (SPI-6). Since its identification, SPI-6 has not had any other characterization of the other open reading frames within this region. My research is concerned with making a series of nonpolar mutations utilizing a technique by Datsenko and Wanner. The effects of these mutations can then be characterized utilizing lacZ reporters cloned into other regulatory genes such as hilE and hilA. Additional experiments for characterizing these mutations effect on SPI-1 function could be done utilizing cell invasion assays. Any effects on Salmonella invasion could then be further characterized by identifying how each of the mutations lead to SPI-1 expression changes. An advantage to this line of research is that the data accumulated from these studies could be applied to other organisms that utilize a type III secretion system. Specifically, I have considered working with the opportunistic pathogen Burkholderia cenocepacia which can cause severe respiratory infections in patients having cystic fibrosis. This pathogen has recently been shown to contain some of the genes found within other type III secretion systems. My interests are to identify the regulatory genes of the apparatus and then to characterize the signal pathways that lead from the environment to the upregulation of the type III secretion system. Regulation of these operons are important since there are many genes involved in encoding the secretion system, therefore it is beneficial to the bacterium to regulate the expression of this system until it has reached a location where expression of the genes would be beneficial to the pathogen. |
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| PUBLICATIONS 1. Picking, W.L., H. Nishioka, P.D. Hearn, M.A. Baxter, A.T. Harrington, A. Blocker, and W.D. Picking. (2005) IpaD of Shigella is independently required for regulation of Ipa protein secretion and efficient insertion of IpaB and IpaC into host membranes. Infection and Immunity 73(3):1432-1440. 2. Baxter, M.A., and B.D. Jones. (2005) The fimYZ gene regulates Salmonella invasion, in addition to type 1 fimbrial expression and bacterial motility. Infection and Immunity 73(3):1377-1385. 3. Baxter, M.A., T.F. Fahlen, R.L. Wilson, and B.D. Jones. (2003) HilE interacts with HilD and negatively regulates hilA transcription and expression of the Salmonella enterica serovar Typhimurium invasive phenotype. Infection and Immunity 71(3):1295-1305. 4. Baxter, M.A., and B.D. Jones. Two-component regulators control hilA expression by controlling fimZ and hilE expression within Salmonella enterica serovar Typhimurium. Infection and Immunity [In Preparation] ORAL PRESENTATIONS
POSTER PRESENTATIONS
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Biomedical Sciences Department |
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Last updated September 03, 2008 |
Copyright (c) 1998 GVSU |