Xiajun Li    Associate Professor, PI
InstituteSchool of Life Science and Technology
Research AreaGenetics and Epigenetics,
Developmental and Stem Cell Biology
Contact Info.Lixj1@@shanghaitech.edu.cn

BS, Peking (Beijing) University, Excellent Graduate
MS, Peking (Beijing) University
PhD, Columbia University, Graduate with distinction
Postdoc, Harvard Medical School
Assistant Professor, Mount Sinai School of Medicine, New York
Associate Professor, Icahn School of Medicine at Mount Sinai, New York

Dr. Li was a graduate of Zhenhai High School of Zhejiang Province. He obtained both his BS and MS degrees from the Biology Department of Peking (Beijing) University. As a graduate student in Columbia University, he worked closely with Dr. Iva Greenwald, an investigator of the renowned Howard Hughes Medical Institute (HHMI) and a member of National Academy of Science (NAS). His doctoral research centered on presenilin proteins involved in Alzheimer’s disease and LIN-12/Notch signaling pathway in C. elegans. After obtaining his PhD degree with distinction from Columbia University, he did his postdoctoral research on embryonic stem (ES) cells in the laboratory of Dr. Philip Leder at Harvard Medical School, an NAS member, a senior HHMI investigator and the founding chair of Genetics Department in Harvard University. Dr. Li established his own laboratory at Mount Sinai School of Medicine of New York University in 2006. He was an associate professor at Icahn School of Medicine at Mount Sinai in New York University before joining ShanghaiTech University in the fall of 2016.

Research Interests
Genomic imprinting is absolutely essential for mammalian development. Dysregulation of genomic imprinting causes a variety of human diseases including cancer, diabetes, cardiovascular diseases and neurological disorders. Dr. Li’s previous study has shown Zfp57 as a master regulator in genomic imprinting. His lab is interested in modeling major human diseases by utilizing Zfp57 mutant mice. Zfp57 is a maternal-zygotic effect gene and loss of Zfp57 causes maternal-zygotic embryonic lethality, the first one identified in mammals. Recently, his lab demonstrated that both maternal and zygotic Zfp57 modulate NOTCH signaling in cardiac development. His future study will be focused on linking genomic imprinting and NOTCH signaling to major human diseases.
Another major research interest of his lab is epigenetic regulation in stem cells, in particular genomic imprinting. Indeed, Zfp57 is critical for the maintenance of genomic imprinting in stem cells, whereas ES cells and iPS cells are promising candidates for cell-based therapies for various degenerative diseases including Alzheimer’s disease. Since genomic imprinting is unstable in these stem cells and loss of genomic imprinting is associated with many human diseases, the ultimate goal of the research is to identify plausible strategies for derivation of ES and iPS cells with relatively stable genomic imprinting that are suitable for future therapeutic applications.

Selected Publications

McDonald C., Liu L., Xiao L., Schaniel C. and Li X. (2016). Genomic imprinting defect in Zfp57 mutant iPS cell lines. Stem Cell Research 16: 259-263.

Lau H., Liu L. and Li X. (2016). Zfp57 mutant ES cell lines directly derived from blastocysts. Stem Cell Research 16: 282-286.

Liu L., Mao S-Q, Ray C., Zhang Y. Bell F., Ng S-F, Xu, G-L and Li X. (2015). Differential regulation of genomic imprinting by TET proteins in embryonic stem cells. Stem Cell Research 15: 435-443.

Shamis Y., Cullen D., Liu L., Yang G., Ng S-F, Xiao L., Bell F., Ray C., Takikawa S., Moskowitz I., Cai C., Yang X. and Li X. (2015). Maternal and zygotic Zfp57 modulate NOTCH signaling in cardiac development. Proc. Natl. Acad. Sci. USA 112(16): E2020-9.

Takikawa S., Ray C., Wang X., Shamis Y., Wu T. and Li X. (2013). Genomic imprinting is variably lost during reprogramming of mouse iPS cells. Stem Cell Research 11(2): 861-873.

Li X. (Invited paper) (2013). Genomic imprinting is a parental effect established in mammalian germ cells. Current Topics in Developmental Biology. 102:35-59.

Zuo X., Sheng J., Lau H., McDonald CM, Andrade M., Cullen DE, Bell FT, Iacovino M., Kyba M., Xu G. andLi X. (2012). The zinc finger protein ZFP57 requires its cofactor to recruit DNA methyltransferases and maintains the DNA methylation imprint in 
embryonic stem cells via its transcriptional repression domain. J. Biol. Chem. 287(3): 2107-18 (Epub 2011 Dec. 5)  (Highlighted in ESC &iPSC News, Top Story from Whitehead Institute).

Li X. *, Ito M., Zhou F., Youngson N., Zuo X., Leder P. and Ferguson-Smith, A. (2008). A maternal-zygotic effect gene, Zfp57, maintains both maternal and paternal imprints. Developmental Cell 15, 547-557 (*, sole corresponding author) (Previewed in Developmental Cell 15: 487-8, 2008).

Li X. and Greenwald I. (1998). Additional evidence for an eight-transmembrane-domain topology for Caenorhabditis elegans  and human presenilins. Proc. Natl. Acad. Sci. USA 95, 7109-7114.

Li X. and Greenwald I. (1997). HOP-1, a Caenorhabditis elegans presenilin, appears to be functionally redundant with SEL-12 presenilin and to facilitate LIN-12 and GLP-1 signaling. Proc. Natl. Acad. Sci. USA 94, 12204-12209.

Li X. and Greenwald I. (1996). Membrane topology of the C. elegans SEL-12 presenilin. Neuron 17, 1015-1021.