Education
2005-2011 PhD, University of Wisconsin-Madison
2003-2005 MA, Boston University
1999-2003 BS, Cheng Kung University, Taiwan
Professional Experience
2017-present Principal Investigator, School of Life Sciences, Peking University
2017-present Principal Investigator, Center for Life Sciences
2011-2017 Postdoctoral Fellow, Whitehead Institute for Biomedical Research/MIT
Honors and Awards
Charles H. Hood Foundation (Charles A. King Trust) Postdoctoral Research Fellowship， 2015
American Heart Association Predoctoral Fellowship， 2009
Teaching
Advanced Cell Biology
The long-term interest of the Lee lab is to understand how stem and progenitor cells integrate multiple environmental signals to make cell-fate decisions under normal and pathological / stressed conditions. While somatic stem cells are often quiescent, lineage-committed progenitor cells play a key role in tissue regeneration and maintaining tissue homeostasis. These lineage-committed progenitor cells with limited self-renewal potential can respond to extrinsic and intrinsic signaling cues, and decide whether to undergo self-renewal or a differentiation division. Blood is one of the tissues with a high capacity of regeneration. Replenishment of RBCs is particularly active in order to ensure sufficient tissue oxygen supply. Therefore, generation of red blood cells (erythropoiesis) represents an ideal system to investigate how dividing progenitor cells maintain self-renewal capacity, and importantly, how self-renewal capacity can be retained or promoted for therapeutic purposes. Our lab uses primary erythroid progenitors as a paradigm to dissect the molecular basis that determines cell self-renewal or differentiation, which will provide insights of developmental decision in normal stem and progenitor cells or leukemic stem cells.
(*Equal contribution)
1. Zhou, Z.*, Zhu, S.*, Hong, Y., Jin, G., Ma, R., Lin, F., Zhang, Y., Lee, H.Y.# and Liu, N.# (2025) Composite transposons with bivalent histone marks function as RNA-dependent enhancers in cell fate regulation. Cell. 188, 1-17. https://doi.org/10.1016/j.cell.2025.07.014
2. Hu, Q.*, Liu, Y.*, Yue, Q., Zhou, S., Jin, X., Lin, F., Huang, X.J., Zhuang, J.#, Lu, J.#, Gao, X.# and Lee, H.Y.# (2024) Lenalidomide-induced pure red cell aplasia is associated with elevated expression of MHC-I molecules on erythrocytes. Nature Communications. 15, 10131. https://doi.org/10.1038/s41467-024-54571-w
3. Liu, Y.*, Nie, X.*, Yao, X.*, Shou, H., Yang, Y., Ge, Y., Tong, X.#, Lee, H.Y.# and Gao, X.# (2024) Developing an erythrocyte-MHC-I conjugate for cancer treatment. Cell Discovery. 10, 99. https://doi.org/10.1038/s41421-024-00713-9
4. Wu, S.*, Deng, Y.*, Sun, H., Liu, X., Zhou, S., Zhao H., Li, H., Guo, F., Yue, Q., Wu, F., Zhao, X., Li, N., Zhu, S., Hu, Q., Xie, S., Zheng, J., Lv, M., Kong, Y., Huang, X.J., Lei, X., Tong, X.# and Gao, X.# and Lee, H.Y.# (2024) BRAF inhibitors enhance erythropoiesis and treat anemia through paradoxical activation of MAPK signaling. Signal Transduction and Targeted Therapy. 9, 338. https://doi.org/10.1038/s41392-024-02033-6
5. Zhu, S.*, Zhang, X.*, Li, N.*, Zhao, X., Li, M., Xie, S., Yue, Q., Li, Y., Li, D., Wu, F., Zhang, Z., Feng, Z., Choi, W., Jia, X., Deng, Y., Hu, Q., Yao, X., Gao, X. and Lee, H.Y. (2024) MED26-enriched condensates drive erythropoiesis through modulating transcription pausing. eLife. https://doi.org/10.7554/eLife.102023.1.sa4
6. Li, D., Zhao, X.Y., Zhou, S., Hu, Q., Wu, F. and Lee H.Y. (2023) Multidimensional profiling reveals GATA1-modulated stage-specific chromatin states and functional associations during human erythropoiesis. Nucleic Acids Research. https://doi.org/10.1093/nar/gkad468
7. Li, D.*, Wu, F.*, Zhou, S., Huang, X.J. and Lee H.Y. (2023) Heterochromatin rewiring and domain disruption-mediated chromatin compaction during erythropoiesis. Nature Structural & Molecular Biology. https://doi.org/10.1038/s41594-023-00939-3
8. Gao, X.*, Lee, H.Y.*, Li, W., Platt, R.J., Barrasa, M.I., Ma, Q., Elmes, R.R., Rosenfeld, M.G. and Lodish, H.F. (2017) Thyroid hormone receptor beta and NCOA4 regulate terminal erythrocyte differentiation. Proceedings of the National Academy of Sciences USA. 114(38), 10107-10112.
9. Gao, X.*, Lee, H.Y.*, da Rocha, E.L., Zhang, C., Lu, Y.F., Li, D., Feng, Y., Ezike, J., Elmes, R.R., Barrasa, M.I., Cahan, P., Li, H., Daley, G.Q. and Lodish, H.F. (2016) TGF-β inhibitors stimulate red cell production by enhancing self-renewal of BFU-E erythroid progenitors. Blood. 128(23), 2637-2641.
10. Lee, H.Y.*, Gao, X.*, Barrasa, M.I., Li, H., Elmes, R.R., Peters, L.L. and Lodish, H.F. (2015) PPAR-α and glucocorticoid receptor synergize to promote erythroid progenitor self-renewal. Nature. 522, 474-7.
11. Lee, H.Y., Johnson, K.D., Boyer, M. E. and Bresnick, E. H. (2011) Relocalizing genetic loci into specific subnuclear neighborhoods. Journal of Biological Chemistry. 286, 18834-18844.
12. Fujiwara, T.*, Lee, H.Y.*, Sanalkumar, R.* and Bresnick, E. H. (2010) Building multifunctionality into a complex containing master regulators of hematopoiesis. Proceedings of the National Academy of Sciences USA. 107, 20429-34.
13. Lee, H.Y., Johnson, K. D., Fujiwara, T., Boyer, M. E., Kim, S.-I. and Bresnick, E. H. (2009) Controlling hematopoiesis through sumoylation-dependent regulation of a GATA factor. Molecular Cell. 36, 984-995.
