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Lawrence T. Reiter, PhD

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 


  • PhD 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

  • Frohlich J, Reiter LT, Saravanapandian V, DiStefano C, Huberty S, Hyde C, Chamberlain S, Bearden CE, Golshani P, Irimia A, Olsen RW, Hipp JF, Jeste SS. Correction to: Mechanisms underlying the EEG biomarker in Dup15q syndrome. Mol Autism. 2019 Nov 6;10:37. doi: 10.1186/s13229-019-0288-y. eCollection 2019. PubMed PMID: 31709034; PubMed Central PMCID: PMC6833208.
  • DiStefano C, Wilson RB, Hyde C, Cook EH, Thibert RL, Reiter LT, Vogel-Farley V, Hipp J, Jeste S. Behavioral characterization of dup15q syndrome: Toward meaningful endpoints for clinical trials. Am J Med Genet A. 2020 Jan;182(1):71-84. doi: 10.1002/ajmg.a.61385. Epub 2019 Oct 26. PubMed PMID: 31654560.
  • Hope KA, Flatten D, Cavitch P, May B, Sutcliffe JS, O'Donnell J, Reiter LT. The Drosophila Gene Sulfateless Modulates Autism-Like Behaviors. Front Genet. 2019 Jun 19;10:574. doi: 10.3389/fgene.2019.00574. eCollection 2019. PubMed PMID: 31316544; PubMed Central PMCID: PMC6611434.
  • Frohlich J, Reiter LT, Saravanapandian V, DiStefano C, Huberty S, Hyde C, Chamberlain S, Bearden CE, Golshani P, Irimia A, Olsen RW, Hipp JF, Jeste SS. Mechanisms underlying the EEG biomarker in Dup15q syndrome. Mol Autism. 2019 Jul 3;10:29. doi: 10.1186/s13229-019-0280-6. eCollection 2019. Erratum in: Mol Autism. 2019 Nov 6;10:37. PubMed PMID: 31312421; PubMed Central PMCID: PMC6609401.
  • Hope KA, McGinn A, Reiter LT. A genome-wide enhancer/suppressor screen for Dube3a interacting genes in Drosophila melanogaster. Sci Rep. 2019 Feb 20;9(1):2382. doi: 10.1038/s41598-019-38663-y. PubMed PMID: 30787400; PubMed Central PMCID: PMC6382765.
  • Toro C, Hori RT, Malicdan MCV, Tifft CJ, Goldstein A, Gahl WA, Adams DR, Fauni HB, Wolfe LA, Xiao J, Khan MM, Tian J, Hope KA, Reiter LT, Tremblay MG, Moss T, Franks AL, Balak C; C4RCD Research Group, LeDoux MS. A recurrent de novo missense mutation in UBTF causes developmental neuroregression. Hum Mol Genet. 2018 Apr 1;27(7):1310. doi: 10.1093/hmg/ddy049. PubMed PMID: 29447355; PubMed Central PMCID: PMC6093340.

View more references (pubmed link)

May 26, 2022