IOANNIS DRAGATSIS, Ph.D., B.S.

Associate Professor
Physiology

Office: 319 TRANSLATIONAL RESEARCH BUILDING
71 SOUTH MANASSAS
MEMPHIS TN 38163
Tel: (901) 448-3615
idragatsis@uthsc.edu

Education

  • Ph.D., Department of Biology, University of Athens, Greece, Department of Biology
  • Ph.D., University of Athens, Greece, Biology
  • B.S., University of Athens, Greece, Pharmaceutical Sciences
  • B.A., University of Athens, Greece , Pharmaceutical Sciences

Research interest/specialty

Role of Huntingtin-associated protein 1 in neonatal feeding. Need for Huntingtin in Mature CNS

Research interest/specialty

Role of Huntingtin-associated protein 1 in neonatal feeding. Need for Huntingtin in Mature CNS

Research keywords

Huntingtin, Huntiongton's Disease, HD, chorea, dementia, CAG, neurodegeneration,

Research description

My laboratory is interested in studying the molecular basis of neurodegenerative diseases using Huntington's Disease (HD) as a model system. HD is an autosomal dominant disorder that affects 1 in 10,000 individuals. HD is characterized by chorea, rigidity and progressive dementia. Symptoms usually begin between the ages of 35 and 50 years, with death typically following 15 to 20 years later. HD is caused by the expansion of an unstable stretch of CAG triplet repeats within the coding region of the HD gene. Moreover the protein encoded by the HD gene, huntingtin, is a novel protein of unknown function. We are using the mouse as a model organism. Inactivation of the mouse homologue of the HD gene results in embryonic lethality demonstrating that huntingtin is essential for early embryonic development. Conditional inactivation of the gene at later stages results in progressive neurodegeneration in the adult mouse, suggesting that huntingtin is also essential for neuronal survival. Analysis of genetically engineered mice provides information in the context of the entire organism, throughout development and in adult organs, and complements in vitro analyses of normal and mutant huntingtin. In addition to providing important practical information regarding a devastating disorder, an analysis of the normal function of huntingtin and its interacting proteins can also provide important basic information regarding normal development and neuronal function in the brain.

Publications

  1. Dragatsis, I, Goldowitz, D, Del Mar, N, Deng, YP, Meade, CA, Liu, L, Sun, Z, Dietrich, P, Yue, J, Reiner, A. CAG repeat lengths > or =335 attenuate the phenotype in the R6/2 Huntington's disease transgenic mouse. Neurobiol Dis, 33 (3), 315-30, 2009.
  2. Dietrich, P, Shanmugasundaram, R, Shuyu, E, Dragatsis, I. Congenital hydrocephalus associated with abnormal subcommissural organ in mice lacking huntingtin in Wnt1 cell lineages. Hum Mol Genet, 18 (1), 142-50, 2009.
  3. Liu, L, Geisert, EE, Frankfurter, A, Spano, AJ, Jiang, CX, Yue, J, Dragatsis, I, Goldowitz, D. A transgenic mouse class-III beta tubulin reporter using yellow fluorescent protein. Genesis, 45 (9), 560-9, 2007.
  4. Dragatsis, I, Zeitlin, S, Dietrich, P. Huntingtin-associated protein 1 (Hap1) mutant mice bypassing the early postnatal lethality are neuroanatomically normal and fertile but display growth retardation. Hum Mol Genet, 13 (24), 3115-25, 2004.
  5. Reiner, A, Dragatsis, I, Zeitlin, S, Goldowitz, D. Wild-type huntingtin plays a role in brain development and neuronal survival. Mol Neurobiol, 28 (3), 259-76, 2003.
  6. Reiner, A, Del Mar, N, Meade, CA, Yang, H, Dragatsis, I, Zeitlin, S, Goldowitz, D. Neurons lacking huntingtin differentially colonize brain and survive in chimeric mice. J Neurosci, 21 (19), 7608-19, 2001.