Tai Min

B.S., Hanyang University, Seoul, Korea, 1984
M.S., Korea Advanced Institute of Science & Technology, 1987
Ph.D., University of Oxford, UK, 1993
Postdoctoral Fellow, California Institute of Technology, 1993-1996
Senior Research Fellow, California Institute of Technology, 1996-1999

Research Interests

Molecular mechanisms of Down syndrome, neurological disorders, and aging

Our work aims to advance the understanding of the underlying molecular mechanisms of normal and dysfunctional neurons affecting distinct brain functions such as memory formation and motor behavior. We are also trying to identify the neuronal circuits responsible for such behaviors.

We are particularly interested in identifying the network of proteins responsible for particular phenotypes in Down syndrome that is caused by full or partial trisomy of human chromosome 21. Down syndrome is a complex disorder that affects about 1 in 700 live births across all ethnic groups. DS patients have various clinical features, but the most common abnormalities include mental retardation, congenital heart disease, craniofacial dysmorphology, hypotonia, and accelerated aging. In particular, a large subset of DS patients develop the pathological and neurochemical changes seen in Alzheimer’s disease by about age 40, and a substantially increased incidence of cataracts at an early age. The exact mechanism underlying those anomalies, however, is not well understood, and the current challenge in the study of Down syndrome is to identify the genes and pathways responsible for the specific manifestations of DS.

Our lab is mainly using Drosophila melanogaster as a model system to understand the roles of genes on chromosome 21 and to elucidate the relationship between genotypes and phenotypes in Down syndrome. Given that many genes expressed in flies and humans are evolutionarily conserved, Drosophila, with its amenability to genetic and behavioral analyses, moderately evolved nervous system, and short generation time, is a valuable tool for investigating the molecular mechanisms of neuronal functions. We also want to take molecules and pathways uncovered in Drosophila and eventually apply this information to the study of Down syndrome. Important cellular regulatory pathways are evolutionarily conserved; thus molecules identified as important regulators of pathology in Drosophila are likely to be regulated similarly in humans. In this context we see Drosophila as a powerful tool for studying the molecular mechanisms of Down syndrome as well as other neurological disorders.

Representative Publications

Griswold, A., Chang, K.T., Runko, A., Knight, M., and Min, K-T. (2007). Sir2 mediates apoptosis through JNK-dependent pathway in Drosophila. Submitted.

Runko, A. and Min, K-T. (2007). Mitochondrial overexpression of frataxin in Drosophila increases resistance to oxidative stress and extends lifespan. Submitted.

Zhang, J., Panicer, L., Nini, L, Min, K-T*, and Simonds W*. (2007). The neuron-specific G protein b5-R7 RGS protein complex regulates redox homeostasis: an evolutionarily conserved defense against oxidative stress. Submitted.

Chang, K.T., and Min, K-T. (2005). Drosophila melanogaster homolog of Down Syndrome Critical Region 1 is critical for mitochondrial function. Nature Neuroscience, 8: 1577-1585.

Menzies, F., Yenisetti, S., Min, K-T. (2005). Roles of Drosophila DJ-1 in oxidative stress and survival of dopaminergic neurons. Current Biology, 6: 1578-1582.

Cho, Y., Griswold, A., Campbell, C., and, Min, K-T. (2005). Individual histone deacetylases in Drosophila modulate transcription of distinct genes. Genomics, 86: 606-617.

Chang, K.T., Shi, Y.J., and Min, K-T. (2003). The Drosophila homolog of human Down’s Syndrome Critical Region 1 gene regulates learning: Implications for mental retardation. Proc. Natl. Acad. Sci. USA, 100: 15794-15799.

Taylor, J.P., Taye, A.A., Campbell, C. Kazemi-Esfarjani, P., Fischbeck, K.H., and Min, K-T. (2003). Aberrant histone acetylation, altered transcription, and retinal degeneration in a Drosophila model of polyglutamine disease are rescued by CREB-binding protein. Genes & Development, 17: 1463-1468.

Pramatarova, A, Ochalski, P.W., Chen, K., Gropman, A, Myers, S., Min, K-T., Howell, B.W. (2003). Nck-b interacts with tyrosine phosphorylated disabled 1 and redistributes in reelin-stimulated neurons. Mol. Cell. Biol., 23: 7210-7221.

Kang, H., Benzer, S., and Min, K-T.(2002). Life extension in Drosophila by feeding a drug. Proc. Natl. Acad. Sci. USA, 99: 838-843.