Lawrence T. Reiter , Ph.D.
Assistant Professor, Department of Neurology
Director, Drosophila Transgenic Core Facility
Education
| B.S. | University of Southern California | 1991 |
| Ph.D. | Baylor College of Medicine | 1997 |
Post-Graduate Training
| Fellowship, Drosophila genetics, University of California, San Diego | 2005 |
Positions and Honors
| Undergraduate Research | Dr. Carol Miller, U.S.C., Los Angeles, CA | 1987-1991 |
| Eighth Grade Teacher | Mc Main School, Orleans Parrish, New Orleans, LA | 1991-1992 |
| Research Associate | Dr. Max Oeschger, L.S.U. Dental School, New Orleans, LA | 1992-1993 |
| Graduate Student | Dr. James R. Lupski, Baylor College of Medicine, Houston, TX | 1993-1997 |
| Postdoctoral Fellow | Dr. James R. Lupski, Baylor College of Medicine, Houston, TX | 1997-1998 |
| Postdoctoral Fellow | Dr. Ethan Bier, U.C.S.D., San Diego, CA | 1999-2005 |
| Assistant Professor | Dept. of Neurology, UTHSC, Memphis, TN | 2005-present |
Research Interests
My laboratory utilizes the powerful genetic model organism Drosophila melanogaster (fruit flies) to investigate the functions of genes involved in human neurological disease. Our main focus is the study of genes related to autism spectrum disorders (ASD). ASDs include the severely debilitating Rett syndrome (RTT) and the mental retardation disorder Angelman syndrome (AS). These syndromes are interrelated at the molecular level and mutations in the gene that causes RTT can also cause AS. In addition, approximately 3 % of all idiopathic autism cases may result from maternally inherited duplications of the region containing the gene that causes AS, UBE3A. Mutations in genes that code for the protein targets of the ubiquitin ligase UBE3A may, therefore, account for a significant percentage of idiopathic autism cases as well.
In our laboratory we utilize Drosophila specific genetic techniques that allow us to generate artificially high levels of normal and mutant fly ube3a proteins in fly heads. Wild type, dominant negative and epitope tagged forms of ube3a are over-expressed in the brains of flies using the GAL4/UAS system in order to increase or decrease the levels of ube3a protein targets. We then identify these targets by 2 D gel electrophoresis and mass spectrometry (proteomics). Potential targets are validated though genetic suppressor/enhancer screens, immunoprecipitation binding assays in 293T cells and immunohistochemistry in the brains of Ube3a null mice. We are also performing both proteomic and genetic screens for proteins directly regulated by Dube3a in the nervous system of flies.
Representative Publications
L. Reiter and E. Bier. 2002. Using Drosophila melanogaster to uncover human disease gene function and potential drug target proteins. Expert Opinion on Therapeutic Targets. 6:387-399.
S. Chien, L. Reiter, E. Bier and M. Gribskov. 2002. Homophila: human disease gene congnates in Drosophila.Nucleic Acids Research 30:149-51.
K. Inoue, K. Dewar, N. Katsanis, L. Reiter, E. Lander, K. Devon, D. Wyman, J. Lupski and B. Birren. 2001. The 1.4-Mb CMT1A duplication/HNPP deletion genomic region reveals unique genome architectrual features and provides insights into the recent evolution of new genes. Genome Research11:1018-1033.
L. Reiter, L. Potocki, M. Gribskov and E. Bier. 2001. A systematic analysis of human disease associated gene sequences in Drosophilamelangaster. Genome Research11:1114-1125.
T. Liehr, L. Reiter, J. Lupski, T. Murakami, U. Cluassen and B. Rautenstrauss. 2001. Regional localization of 10 mariner transposon-like ESTs by means of FISH-evidence for a correlation with fragile sites. Mammalian Genome 12:326-328.
L. Reiter , T. Liehr, B. Rautenstrauss, H. Robertson and J. Lupski. 1999. Human recomination-associated genomic disorders appear to coincide with locations of mariner transposons. Genome Research 9:839-843.
L . Reiter , E. Nelis, P. De Jonhge, C. Van Broekhoven and J. Lupski. 1998. Human meiotic recombination products revealed by sequencing a hotspot for homologous strand exchange in multiple HNPP deletion patients. American Journal of Human Genetics62:1023-1033.
V. Timmerman, B. Rautenstrauss, L. Reiter, T. Koeuth, A. Löfgren, T. Leihr, E. Nelis, K. Bathke, P. De Jonghe, H. Grehl, J.- J. Martin, J. Lupski and C. Van Broeckhoven. 1997. Detection of the CMT1A/HNPP recombination "hotspot" in unrelated patients of European descent. Journal of Medical Genetics34:43-49.
T. Murakami, L. Reiter and J. Lupski. 1997. Genomic structure and expression of the human heme A:farnesyltransferase (COX10) gene. Genomics 42:161-164.
L. Reiter , T. Murakami, T. Koeuth, R. Gibbs and J. Lupski. 1997. The human COX10 gene is disrupted during homologous recombination between the 24-Kb proximal and distal CMT1A-REPs. Human Molecular Genetics 6:1595-1603.
L. Reiter , T. Murakami, T. Koeuth, L. Pentao, M. Muzny, R. Gibbs and J. Lupski. 1996. A recombination hotspot responsible for two inherited peripheral neuropathies is located near a mariner transposon-like element. Nature Genetics12:288-297.
L. Reiter , D. Steffen, S. Shapira, J. Lupski, M. Frazier and D. Wheeler. 1995. A searchable video database of dysmorphology. Journal of the American Medical Informatics Association (symposium supplement SCAMC Proceedings), p. 1000.
J. Hubar, M. Oeschger and L. Reiter. 1994. Effectiveness of radiographic film barrier envelopes. General Dentistry 42:406-408