Lawrence T. Reiter, Ph.D.

Lawrence T. Reiter, Ph.D.

Associate Professor
Department of Neurology
Department of Anatomy and Neurobiology

The University of Tennessee Health Science Center
855 Monroe Avenue, Suite 415
Memphis, TN 38163
Phone: (901) 448-2635
Office: (901) 448-7443
Fax: (901) 448-7440
Lab: 431 Johnson Building
Email: Lawrence T. Reiter


  • Ph.D. Institution: Department of Cell and Molecular Biology, Baylor College of Medicine
  • Postdoctoral: University of California San Diego


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 Angelman syndrome and autism spectrum disorders. These disorders are interrelated at the molecular level and one of the goals of our laboratory is to identify genes and proteins regulated by one or more of the proteins that, when mutated, can cause and autism phenotype. In addition, approximately 3-5 % of all autism cases result from maternally derived duplications of the region containing the gene that causes AS, UBE3A. Mutations in the protein targets of the ubiquitin ligase UBE3A may therefore account for a significant percentage of idiopathic autism cases.

In our laboratory we utilize Drosophila specific genetic techniques that allow us to generate artificially high levels of normal and mutant fly Dube3a 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 have now identified 50 of these potential Dube3a regulated proteins and are actively validating these interactions using whole genome molecular methods (genomics), genetic suppressor/enhancer screens, immunostaining in fly neurons (immunoflourescence), and changes in synaptic function and stability at the fly neuromuscular junction (electrophysiology). Using these methodologies in flies we have identified Dube3a regulation of the actin cytoskeleton (Reiter et al. Hum Mol Genet. 2006 Sep 15;15(18):2825-35) as well as the synthesis of monoamines (Ferdousy et al Neurobiol Dis. 2011 Mar;41(3):669-77).

Another aspect of our work is related to describing various quantifiable behavior phenotypes in Ube3a deficient and over-expressing mice. Specifically, we are interested in abnormal social behavior (a measure of autistic behavior in mice) as well as abnormal fluid licking behavior (a natural behavior which reflects cerebellar function). These experiments have already shown that Ube3a deficient animals have measurable deficits in fluid licking that are directly related to the decrease in Ube3a levels in the brain (Heck et al. Hum Mol Genet. 17(14):2181-9) as well as hypoactivity and defects in exploratory behavior in the Ube3a deficient animals (Allensworth et al. BMC Genet. 2011 Jan 14;12:7).

Finally, we have been doing in depth phenotypic and molecular analysis of individuals with interstitial duplication 15q autism. Since 2007 we have been collecting a variety of language, neuropsychiatric, neurological and gene expression data from subjects with interstitial 15q chromosomal duplications. We hope that our basic research into the functional targets of UBE3A will lead to a better understanding of the phenotypes in this particular autism population where the UBE3A gene is duplicated, and presumably expressed at higher levels than in unaffected individuals. For more information on our clinical study see As an extension of this work which bridges the gap between basic and clinical research, we recently began an NIH funded study to generate dental pulp derived neruons from individuals with either the Angelman syndrome deletion in this region or a duplication of this region on chromosome 15q causing autism. We hope that these patient-derive neuronal cultures will allow us to perform more in depth molecular and electrophysiological analysis of both conditions in the near future. For more information on the dental pulp stem cell study please see

Representative Publications

  • Hope KA, LeDoux MS, Reiter LT. The Drosophila melanogaster homolog of UBE3A is not imprinted in neurons. Epigenetics. 2016 Aug 11:1-6. [Epub ahead of print] PubMed PMID: 27599063; PubMed Central PMCID: PMC5048722.
  • Finucane BM, Lusk L, Arkilo D, Chamberlain S, Devinsky O, Dindot S, Jeste SS, LaSalle JM, Reiter LT, Schanen NC, Spence SJ, Thibert RL, Calvert G, Luchsinger K, Cook EH. 15q Duplication Syndrome and Related Disorders. 2016 Jun 16. In: Pagon RA, Adam MP, Ardinger HH, Wallace SE, Amemiya A, Bean LJH, Bird TD, Ledbetter N, Mefford HC, Smith RJH, Stephens K, editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2016. Available from PubMed PMID: 27308687.
  • DiStefano C, Gulsrud A, Huberty S, Kasari C, Cook E, Reiter LT, Thibert R, Jeste SS. Identification of a distinct developmental and behavioral profile in children with Dup15q syndrome. J Neurodev Disord. 2016 May 6;8:19. doi: 10.1186/s11689-016-9152-y. PubMed PMID: 27158270; PubMed Central PMCID: PMC4858912.
  • Ikbale el-A, Goorha S, Reiter LT, Miranda-Carboni GA. Effects of hTERT immortalization on osteogenic and adipogenic differentiation of dental pulp stem cells. Data Brief. 2016 Jan 14;6:696-9. doi: 10.1016/j.dib.2016.01.009. PubMed PMID: 26958627; PubMed Central PMCID: PMC4773409.
  • Urraca N, Memon R, El-Iyachi I, Goorha S, Valdez C, Tran QT, Scroggs R, Miranda-Carboni GA, Donaldson M, Bridges D, Reiter LT. Characterization of neurons from immortalized dental pulp stem cells for the study of neurogenetic disorders. Stem Cell Res. 2015 Nov;15(3):722-30. doi: 10.1016/j.scr.2015.11.004. PubMed PMID: 26599327; PubMed Central PMCID: PMC4698085.
  • LaSalle JM, Reiter LT, Chamberlain SJ. Epigenetic regulation of UBE3A and roles in human neurodevelopmental disorders. Epigenomics. 2015 Oct;7(7):1213-28. doi: 10.2217/epi.15.70. Review. PubMed PMID: 26585570; PubMed Central PMCID: PMC4709177.

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