Li, Xiaodong, Ph.D.
College of Life Sciences, WuHan University, Hubei Province, P.R.China 430072
86-027-68753585(O), 86-027-68752560(Fax)， firstname.lastname@example.org
1993/9-1997/7: Peking Univ., B.S. in Biochemistry and Molecular Biology
1997/9- 2002/9: Northeastern Univ., MA, USA. Ph.D. in Cell Biology
2002/10-2004/10:Harvard Medical School, postdoc in Neurology
2004/12 –： WuHan Univ., College of Life Sciences (Neurobiology and Physiology)
1.Kramer A, Yang FC, Snodgrass P, Li X, Scammell TE, Davis FC, Weitz CJ. Regulation of daily locomotor activity and sleep by hypothalamic EGF receptor signaling. Science. 294:2511-5（2001）
2．Li X, Sankrithi N, Davis FC. Transforming growth factor-alpha is expressed in astrocytes of the suprachiasmatic nucleus in hamster: role of glial cells in circadian clocks. NeuroReport. 13(16):2143-7（2002）
3．Kramer A, Yang FC, Snodgrass P, Li X, Scammell TE, Davis FC, Weitz CJ. Regulation of daily locomotor activity and sleep by hypothalamic EGF receptor signalling. Novartis Found Symp. 253:250-62; discussion 102-9, 263-6, 281-4（2003）
4．Li X, Gilbert J, Davis FC. Disruption of masking by hypothalamic lesions in Syrian hamsters. J Comp Physiol. 191(1):23-30（2005）
5．Li X, Davis FC. Developmental expression of 3 clock genes in the Syrian hamster. Dev Brain Res.158(1-2):31-40(2005)
6．Ding Q,Li X*. Neural pathway for fever generation. Neurosci bulletin. 22（6）：350-354(2006)
7. Ji YT, Li X*. Cloning and developmental expression analysis of PK2 and PKR2 in the suprachiasmatic nucleus of the Syrian hamster. Brain Res. 1271: 18-26(2009)
8. Yoshida K,Li X, Cano G, Lazarus M,Saper CB. Parallel preoptic pathways for the inhibition of thermogenesis. J Neurosci 29(38):11954-64(2009)
1.Distinguished Young Scientist Fund, Hubei Province(PI）
3.State Key Research Project“Establishment and Application of Mouse Models for Human diseases”（participating）
4.China MOE New Scholar Fund（PI，2008/1-2009/12）
5. NSFC Key project 30830112 （2009/1-2012/12）（participating）
6.China MOST Key Research Project “Proteomics and Peptidomics Research on Depression(2009/1-2012/12, participating）
7. NSFC30970953 PI，2010/1-2012/12）
The lab is aiming to address the neurobiological mechanisms underlying circaidian rhythms generation at the systems neuroscience level. We use model animals including mouse, rat and Syrian hamsters. Transgenic, condictional gene knockout, viral-vector mediated RNAi, viral vector mediated specific cell killing, tract tracing and behavioral and physiological telemetry recording techniques are applied. We also study the involvement of epigenetic mechanisms in clock genes’ developmental expression. Several lines of work are currently performed:
1. Neurobiological basis of biological rhythms.
This represents work focused on the PK2/PKR2 signaling pair and their involvement in circadian rhythms generation and transmission in different hypothalamic nuclei. We use AAV-RNAi to achieve site-specific PKR2 knockdown in the suprachiasmatic nucleus to address its role in rhythm generation within the SCN. We use traditional (CTB, FG, BDA) and novel (AAV and lentiviral vectors) tract tracing techniques to investigate the connections of PKR2-expressing neurons in the hypothalamic PVH, DMH, we use AAV-RNAi as well as lentiviral vector mediated cell specific killing to study those cells’ involvment in biological rhythms.
2. Epigenetic mechanisms in clock genes’ developmental expression control.
We are analyzing promoter DNA methylation changes during devlelopment and studing the involvement of epigenetic mechanisms in clock genes’developmental expression changes.
3. Contributions of specific SCN neuroal types to biological rhythms using condiction gene KO mice.
Using BMAL1 conditional KO mice and different transgenic Cre mice, we want
to KO BMAL1 gene within specific SCN neurons. This approach will help us to
determine the specific contribution of each cell type within the SCN to the overt
biological rhythms of the animal.
4. Transcriptome, proteome and secretome studies on immortalized SCN cells
We are constructing lentiviral vectors driving GFP expression under specific promoters. Using these vectors, the SCN2.2 cell line can be sorted using FACS to pure populations of neurons of different chemical phenotype. Their difference can be analyzed using microarray and proteomics techniques. SCN lesion/transplantation model can be used to study the functions of each cell types.