Dr. Wang's research interest is in the area of the regulation of cell cycle and the response to the expression of damaged proteins. He teaches medical students in basic sciences in small group sessions. He also teaches graduate students for Bioregulation and Research techniques.
Dr. Wang came to the FSU College of Medicine from Baylor College of Medicine, where he was a postdoctoral fellow. He obtained his Ph.D. degree from the University of Virginia in 1997.
Ph.D., University of Virginia, Charlottesville, Va., 1993 - 1997
Postdoctoral fellow, HHMI, Baylor College of Medicine, Houston, Texas, 1997 - 2002
FSU University Service
Member, Council on Research and Creativity (2009–present).
FSU Department Service
Chair, Faculty Search Committee (2009–present).
Editorial Board Membership(s)
PLoS One (2011–present).
Chinese Journal of Biotechnology (2008–present).
Guest Reviewer for Refereed Journals
EMBO reports; J. Cell Biology; PLoS One; Molecular Biology of the Cell; Molecular Systems Biology;Genetics; Cell Cycle; EMBO Journal; PLoS Genetics; Cell Biology International; Proceedings of the National Academy of Sciences
Reviewer or Panelist for Grant Applications
ANR, France (2011).
Welcome Trust (2010–2011). v
MRC-CDA, UK (2010).
CEGR, Hong Kong (2008–2009).
NSFC, China (2007).
1. The Leukemia & Lymphoma Society Special Fellow, 2001-2004
2. Andrew Fleming Award for outstanding dissertation, 1997, Department of Biology, University of Virginia
3. Young Scientist Award, 1996, FASEB meeting, Snowmass, Colorado
4. The Royal Society Fellowship, 1992-1993, Cambridge University
The American Society for Cell Biology
American Society for Microbiology
American Society for Genetics
THE REGULATION OF CELL CYCLE TRANSITION:
One research interest in this lab is to understand the coordination of spindle elongation and chromosome segregation by using budding yeast Saccharomyces cerevisiae as an experimental model system. Cyclin dependent kinase (CDK) is the key regulator of cell cycle progression and two signaling pathways called FEAR and MEN are responsible for the inactivation of cyclin dependent kinase (CDK) after chromosome segregation. We are currently investigating how the temporal inactivation of CDK controls the timing of spindle elongation, which is critical for faithful chromosome segregation.
THE SILENCING OF THE SPINDLE ASSEMBLY CHECKPOINT:
It is well established that incorrect kinetochore-microtubule activates the spindle assembly checkpoint (SAC) to delay cell cycle progression, a mechanism essential for segregation of sister chromatids to daughter cells. However, we know little how this activated checkpoint is silenced after cells established correct chromosome attachment. We are testing how the establishment of correct kinetochore-microtubule interaction deactivates this checkpoint. Defect in this regulation will lead to chromosome mis-segregation and generate aneuploidy, which has been shown to contribute to cancer development.
THE CELLULAR RESPONSE TO THE EXPRESSION OF DAMAGED PROTEINS:
Misfolded proteins can be refolded with the assistance of chaperones or degraded through the proteasome. When too much misfolded proteins are present, they aggregate and form a structure called aggresome, which not only decreases the toxicity of the misfolded proteins but also facilitates their clearance by autophagy. Failure of this process is responsible for the accumulation of unfolded proteins that causes cell death in neurodegenerative diseases. Using budding yeast as a model system, we have identified many genes involved in aggresome formation and we are investigating the molecular function of these genes in the response to the expression of misfolded proteins.
Fengzhi, J., Hong, L., Ping, L., Hong-Guo, Y., & Wang, Y. (2012). Loss of function of the Cik1/Kar3 motor complex results in chromosomes with syntelic attachment that are sensed by the tension checkpoint. PLoS Genetics, 8, e1002492.
Liu, H., Jin, F., Liang, F., Tian, X., & Wang, Y. (2011). The Cik1/Kar3 Motor Complex Is Required for the Proper Kinetochore-Microtubule Interaction After Stressful DNA Replication. Genetics, 187(2), 397-U58.
Wang, Y. (2010). A new layer of regulation is required to silence the DNA damage checkpoint. Cell Cycle, 9(18), 3642-3642.
Baldwin, M. L., Julius, J. A., Tang, X., Wang, Y., & Bachant, J. (2009). The yeast SUMO isopeptidase Smt4/Ulp2 and the polo kinase Cdc5 act in an opposing fashion to regulate sumoylation in mitosis and cohesion at centromeres. Cell Cycle, 8(20), 3406-3419.
Liang, F., Jin, F., Liu, H., & Wang, Y. (2009). The Molecular Function of the Yeast Polo-like Kinase Cdc5 in Cdc14 Release during Early Anaphase. Mol Biol Cell, 20(16), 3671-3679.
Zhang, J., Li, Y., Guo, L., Cao, R., Zhao, P., Jiang, W., Ma, Q., Yi, H., Li, Z., Jiang, J., Wu, J., Wang, Y., & Si, S. (2009). DH166, a beta-carboline derivative, inhibits the kinase activity of PLK1. Cancer Biol Ther, 8(24), 2374-2383.
Fu, Da-Hua, Jiang, W., Zheng, Jian-Ting, Zhao, Gui-Yu, Li, Y., Yi, H., Li, Zhuo-Rong, Jiang, Jian-Dong, Yang, Ke-Qian, Wang, Y., & Si, Shu-Yi. (2008). Jadomycin B, an Aurora-B kinase inhibitor discovered through virtual screening. Mol Cancer Ther, 7(8), 2386-2393.
Hong Liu, Fengshan Liang, Fengzhi Jin and Yanchang Wang. (2008) The coordination of centromere replication, spindle formation and kinetochore-microtubule interaction in budding yeast. PLoS Genetics. 4:e1000262. Epub 2008 Nov 21.
Fengzhi Jin, Hong Liu, Fengshan Liang, Raed Rizkallah, Myra M. Hurt and Yanchang Wang (2008) Temporal control of the dephosphorylation of Cdk substrates by mitotic exit pathways in budding yeast. Proc Natl Acad Sci U S A. 105:16177-82
Fengshan Liang and Yanchang Wang (2007) DNA damage checkpoints inhibit mitotic exit by two different pathways. Molecular and Cellular Biology 14:5067-5078
Yan Li, Fengshan Liang, Wei Jiang, Fusheng Yu, Rihui Cao, Qinghe Ma, Xiuyong Dai, Jiandong Jiang, Yanchang Wang*, and Shuyi Si* (2007) DH334, a Beta-carboline anti-cancer drug, inhibits the CDK activity of budding yeast. Cancer Biology and Therapy 6(8) [Epub ahead of print] *co-corresponding author
Tang X. and Wang Y. (2006) Pds1/Esp1 dependent and independent sister chromatid separation in mutants defective for protein phosphatase 2A. Proc Natl Acad Sci U S A. 103:16290-16295
Liu H. and Wang Y. (2006) The Function and Regulation of Budding Yeast Swe1 in Response to Interrupted DNA Synthesis. Mol Biol Cell. 17:2746-56 (Epub Mar. 2006)
Wang Y. and Ng T. (2006) Phosphatase 2A negatively regulates mitotic exit in Saccharomyces cerevisiae. Mol. Biol Cell 17(1) 80-89 (Epub Aug. 2005)
Wang Y, Shirogane T, Liu D, Harper JW, Elledge SJ. (2003) Exit from exit: resetting the cell cycle through Amn1 inhibition of G-protein signaling. Cell 112 (5):697-709
Hu F*, Wang Y*, Liu D, Li Y, Qin J, Elledge SJ. (2001) Regulation of the Bub2/Bfa1 GAP complex by Cdc5 and cell cycle checkpoints. Cell 107(5):655-65. (*equal contributor)
Wang Y*, Hu F*, Elledge SJ. (2000) The Bfa1/Bub2 GAP complex comprises a universal checkpoint required to prevent mitotic exit. Curr Biol. 2000 10(21):1379-82. (* equal contributor)
Wang Y, Burke DJ. (1997) Cdc55p, the B-type regulatory subunit of protein phosphatase 2A, has multiple functions in mitosis and is required for the kinetochore/spindle checkpoint in Saccharomyces cerevisiae. Mol Cell Biol. 17:620-6.
Wang Y, Burke DJ. (1995) Checkpoint genes required to delay cell division in response to nocodazole respond to impaired kinetochore function in the yeast Saccharomyces cerevisiae. Mol Cell Biol 15:6838-44