Associate Professor

Ph.D., University of Oxford, 1993
Postdoctoral fellow, California Institute of Technology, 1993 - 1999
Staff Scientist, California Institute of Technology, 1999 - 2000
Principal Investigator, NINDS, NIH, 2000 - 2007

Program Affiliation: Molecular Biology & Genetics

Research Groups Affiliation: Behavior | Biochemistry | Cell Biology | Development | Evo-Devo | Genetics

Phone: 812/856-0962
Fax: 812/855-6082
Email Tai

FlyIU website

Our work aims to understand the underlying molecular and cellular mechanisms of normal and dysfunctional neurons affecting distinct brain functions such as learning and memory.  To this end, we are using several different model systems including primary cell cultures, Drosophila, and mice.  We are also using various techniques: molecular biology, cell biology, biochemistry, genetics, electrophysiology, and imaging to address our questions.

Down Syndrome
We are taking a novel approach to study Down syndrome (caused by full or partial trisomy of human chromosome21), which is using Drosophila as a model system.  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, has been a valuable tool for studying various biological questions.  We believe that Drosophila model can provide a unique opportunity to understand the underlying geneotype-phenotype relationship in DS, for which other model systems have had limited success.  Using powerful Drosophila genetic tools, we can overexpress individual or multiple genes sharing spatio-temporal expression pattern or involved in the same pathways, and then systematically characterize the resulting phenotypes.  We will be able to identify individual genes or a subset of key genes that are responsible for specific phenotypes seen in DS. 

Mitochondrial Dynamics
Mitochondria are dynamic organelles that undergo constant morphological changes through fission and fusion as well as move between different sub-cellular regions.  We have generated various new tools to label, chase, and impair mitochondria under specific conditions in vivo.  We are currently studying the molecular and cellular mechanisms that regulate mitochondrial dynamics and transportation in normal neurons as well as disease state of neurons.

Synaptic Functions
Proteins involved in mRNA trafficking and local protein synthesis play important roles in morphogenesis of dendritic spines and in the formation of memories.  We are interested in understanding the molecular mechanisms of local protein synthesis using mouse primary hippocampal cell cultures and animal models.

Chang, K, and Min, K-T. (2009). Up-regulation of three Drosophila homologs of human chromosome 21 genes alters synaptic function: implications for Down syndrome. Proc. Natl. Acad. Sci. USA. doi:10.1073/pnas.0906510106

Griswold, A., Chang, K.T., Runko, A., Knight, M., and Min, K-T. (2008). Sir2 mediates apoptosis through JNK-dependent pathway in Drosophila. Proc. Natl. Acad. Sci. USA.105. 8673-8678.

Runko, A., Griswold, A, and Min, K-T. (2008). Overexpression of frataxin in the mitochondria increases resistance to oxidative stress and extends lifespan in Drosophila. FEBS Letters, 582, 715-719.

Davies K. J, Ermak G, Rothermel BA, Pritchard M, Heitman J, Ahnn J, Henrique-Silva F, Crawford D, Canaider S, Strippoli P, Carinci P, Min K-T, et al. (2007). Renaming the DSCR1/Adapt78 gene family as RCAN: regulators of calcineurin. FASEB J. 21, 3023-3-28.

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.

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.

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.

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.