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Tsai, Chih-Cheng Ph.D.

Photograh of Chih-Cheng Tsai, PhD

Associate Professor
PhD, SUNY-Stony Brook, 1994

Phone: (732) 235-4885
Fax: (732) 235-5038


Research Interest: Roles of transcriptional cofactors and their dependent pathways in regulating Drosophila development and causing human diseases.

During animal development, accurately timed repression of gene expression is as important as activation. Aberrant transcriptional repression or activation caused by changes in environmental factors or growth factors or by mutations often leads to developmental defects or diseases. Emerging evidence indicates that environmental factors, signaling transduction pathways and therapeutic compounds can influence the transcriptional output of multiple transcriptional factors by affecting their shared transcriptional corepressors or chromatin modifying factors. My laboratory studies the in vivo and in vitro properties of three different but functionally connected transcriptional corepressor families, namely Atrophin/RERE, SMRTER/SMRT, and Ataxin-1/Brother of Ataxin-1.

Since these transcriptional cofactors are conserved in evolution, my lab employs a combination of the Drosophila system and cultured human cells for our studies. We place specific emphasis on how these transcriptional cofactors, aided by their respective associated chromatin modifying factors, influence the Notch, EGFR, and nuclear receptor regulatory pathways during Drosophila development. Our recent discoveries show that these three transcriptional corepressors converge in regulating Drosophila wing, ovary, and sensory organ development, allowing us to use these well-established developmental pathways in our studies. Our long-term goal is to apply the knowledge that we learn from fly to the mammalian systems, since human homologs of these Drosophila transcriptional corepressors are implicated in numerous diseases, including neurodegenerative disorders and cancers.

Selected Publications:

  • Heck, W. B., Zhang, B., Tong, X., Pan, Z., Deng, W.-M., Tsai, C.-C. The transcriptional corepressor SMRTER influences both Notch and ecdysone signaling during Drosophila development. Biology Open, 1:182-196 (2012). Cover article.

  • Tong, X., Gui, H., Jin, F., Heck, B.W., Lin, P., Ma, J., Fondell, JD, and Tsai, C.-C.Ataxin-1 and Brother of Ataxin-1 are components of the Notch signaling pathway EMBO Rep. 12 (5): 428-35 (2011). Faculty of 1000 article.

  • Gui, H., Li, M.-L., Tsai, C.-C. A Tale of Tailless. Developmental Neuroscience 33(1):1-13 (2011).

  • Wang, L. and Tsai, C.-C. Atrophin proteins: An overview of a new class of nuclear receptor corepressors. Nuclear Receptor Signaling, 6, e009 (2008). Review article.

  • Wang, L., Charroux, B., Kerridge, S., Tsai., C.-C. Atrophin recruits HDAC1/2 and G9a to modify histone H3K9 and to determine cell fates. EMBO Rep. 9, 6, 555-562 (2008). Cover article.

  • Wang, L., Rajan, H., Pitman, J.L., McKeown, M.M., Tsai, C.-C. Histone deacetylase-associating Atrophin proteins are nuclear receptor co-repressors. Genes & Development 20, 525-530 (2006).

  • Mizutani, A., Rajan, H., Wang, L., Vig, PJS, Alaynick, WA, Thaler, JP, Tsai, C.-C. Boat, an AXH domain protein, suppresses the cytotoxicity of mutant ataxin-1. EMBO Journal 24, 3339-51 (2005).

  • Tsai, C.-C., Kao, H.-Y., Mizutani, A., Banayo, E., Rajan. H., McKeown M., and Evans, R. M. Ataxin-1, a SCA1 neurodegenerative disorder protein, is functionally linked to the transcriptional co-repressor of retinoid and thyroid hormone receptors. Proc Natl Acad Sci USA 101, 4047-4052 (2004). Faculty of 1000 article.

  • Tsai, C.-C. and Fondell, J. Nuclear receptor recruitment of histone-modifying enzymes to target gene promoters. Vitam Horm. 93-122 (2004). Review article.

  • Tsai, C.-C., Kao, H.-Y., Yao, T.-P., McKeown, M., Evans, R. M. SMRTER, a Drosophila nuclear receptor co-regulator, reveals that EcR-mediated repression is critical for development. Molecular Cell 4, 175-186 (1999). Cover article.


  • Biochemistry
  • Neuroscience
  • Cell and Developmental Biology
  • Physiology and Integrative Biology

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