Home /
yuxiang01(AT)pku.edu.cn
YU,Xiang
Title:
Professor
Office Phone: 57531
Office Address: LUI CHE WOO BUILDING,Peking University, No.5 Yiheyuan Road, Haidian District,Beijing, P.R.China 100871
Lab Phone: 58685
Lab Address: LUI CHE WOO BUILDING,Peking University, No.5 Yiheyuan Road, Haidian District,Beijing, P.R.China 100871
Lab Homepage: http://
Personal Homepage: http://
Resume
Education
1995-1999 Ph.D., MRC Laboratory of Molecular Biology and Trinity College, University of
Cambridge, UK.
1999 M.A. Cantab., Trinity College, University of Cambridge, UK.
1992-1995 B.A. Cantab., Trinity College, University of Cambridge, UK.
Professional Experience
2019-present Professor, School of Life Sciences, Peking University
2019-present Investigator, Peking University-Tsinghua University Center for Life Sciences
2019-present Investigator, IDG/McGovern Institute for Brain Research at Peking University
2019-present Director, Autism Research Center, Peking University Health Science Center
2014-2019 Senior Investigator, Institute of Neuroscience, Chinese Academy of Sciences
2005-2014 Investigator, Institute of Neuroscience, Chinese Academy of Sciences
2005 Grass Fellow, Marine Biological Laboratory
1999-2005 Post-doctoral fellow, Stanford University Medical Center
Honors and Awards
2019 Hsiang-tung Chang Young Neuroscientist Award
2017 Ten Thousand Talent Program, Science and Technology Innovation Leader
2017 Shanghai Leading Talent
2017 Excellent Graduate Advisor of the Chinese Academy of Sciences
2016 Shanghai Subject Chief Scientist
2016 Young Science and Technology Innovation Leader, Ministry of Science and Technology of China
2014 China Young Women Scientists’ Award
2014 Shanghai Talented Young Scientist Award
2012 Excellent Graduate Advisor of the Chinese Academy of Sciences
2011 National Science Fund for Distinguished Young Scholars
Research Interests
Mechanisms underlying neural circuit development and plasticity

The normal functioning of the brain relies on its intricate and complex circuits. Natural sensory experience is critical to the neuronal morphogenesis, synaptogenesis and the formation of functional neural circuits. In previous work, we showed the early developing brain exhibits different plasticity rules, as compared to the mature brain. Specifically, we showed: 1) early sensory experience globally and cross-modally regulates the development of multiple sensory cortices, in a mechanism mediated by the neuropeptide oxytocin; 2) during early neuroinflammation, perivascular pericytes rapidly sense the inflammatory signal and release the cytokine CCL2, which in turn, increase excitatory synaptic transmission in multiple brain regions; 3) during neural circuit maturation in the adolescent brain, sensory experience coordinately regulates the maturation of “useful” spines and the pruning of “less used” spines, in a mechanism dependent on the limited resource, the cadherin/catenin cell adhesion complex.

Based on these results, we proposed the “early global cross-modal neural circuit development hypothesis”. It is well known that the early developing brain is more plastic, and that some brain regions have critical periods. However, the underlying mechanisms are not well understood. We use a combination of single cell expression profiling, molecular biology, genetics and immunohistochemistry to investigate the molecular mechanisms underlying this type of plasticity. We also use electrophysiology, optical imaging and behavioral assays to identify the cellular and circuit mechanisms through which sensory experience and environmental factors regulates the early development of neurons, glial cells and the neurovascular unit. Understanding early global cross-modal plasticity mechanisms in the developing brain is critical to our understanding of the basic mechanism of brain wiring. Developmental neurological disorders, such as autism spectrum disorders and intellectual disabilities, have devastating impacts on the well-being of affected children. By understanding the operating principles of the young brain, early individualized interventions, through either drug therapies or behavioral training, can be developed, with important clinical and social implications.
Representative Peer-Reviewed Publications
Original articles
1. Duan, L., Zhang, X.D., Miao, W.Y., Sun, Y.J., Xiong, G., Wu, Q., Li, G., Yang, P., Yu, H., Li, H., Wang, Y., Zhang, M., Hu, L.Y., Tong, X., Zhou, W.H., Yu, X.* (2018) PDGFRβ cells rapidly relay inflammatory signal from the circulatory system to neurons via chemokine CCL2. Neuron 100(1):183-200. (highlighted by same issue Preview 100(1):11-13)
2. Hu C.C., Xu X.*, Xiong G.L., Xu Q., Zhou B.R., Li C.Y., Qin Q., Liu C.X., Li H.P., Sun Y.J.*, Yu X.* (2018) Alterations in plasma cytokine levels in Chinese children with autism spectrum disorder. Autism Research 11(7):989-999
3. Li M.Y., Miao W.Y., Wu Q.Z., He S.J., Yan G., Yang Y., Liu J.J., Taketo M.M. and Yu, X.* (2017) A critical role of presynaptic Cadherin/Catenin/p140cap complexes in stabilizing spines and functional synapses in the neocortex. Neuron 94(6):1155-1172
4. Wang Q., Shen F.Y., Zou R., Zheng J.J., Yu X.*, Wang Y.W.* (2017) Ketamine-induced apoptosis in the mouse cerebral cortex follows similar characteristic of physiological apoptosis and can be regulated by neuronal activity. Mol. Brain 10(1):24. doi: 10.1186/s13041-017-0302-2.
5. Liu H., Sang S., Lu Y., Wang Z., Yu X.*, and Zhong C.* (2017) Thiamine metabolism is critical for regulating correlated growth of dendrite arbors and neuronal somata. Sci. Rep. 7(1):5342 doi: 10.1038/s41598-017-05476-w.
6. Wang L., Li M.Y., Qu C., Miao W.Y., Yin Q, Liao J., Cao H.T., Huang M., Wang K., Zuo E., Peng G., Zhang S.X., Chen G., Li Q., Tang K., Yu Q., Li Z., Wong CCL, Xu G., Jing N., Yu X.*, and Li J*. (2017) CRISPR-Cas9-mediated genome editing in one blastomere of two-cell embryos reveals a novel Tet3 function in regulating neocortical development. Cell Res. 27(6):815-829
7. Wang M., Li H., Takumi T., Qiu Z., Xu X.*, Yu X.* and Bian W.J.* (2017) Distinct Defects in Spine Formation or Pruning in Two Gene Duplication Mouse Models of Autism Neurosci. Bull. 33(2):143-152
8. Zhang S.X., Duan L.H., He S.J., Zhuang G.F. and Yu X.* (2017) Phosphatidylinositol 3,4-bisphosphate regulates neurite initiation and dendrite morphogenesis via actin aggregation. Cell Res. 27(2):253-273.
9. Zhang S.X., Duan L.H. and Yu, X.* (2016) Actin Aggregations Mark the Sites of Neurite Initiation. Neurosci. Bull. 32(1): 1-15.
10. Bian W.J., Miao W.Y., He S.J., Qiu Z. and Yu, X.* (2015) Coordinated spine pruning and maturation mediated by inter-spine competition for cadherin/catenin complexes. Cell 162(4): 808-822 [highlighted by Nat. Rev. Neurosci. 16(10):577; selected as “exceptional” by Faculty 1000]
11. Bian W.J., Miao W.Y., He S.J., Wan Z.F., Luo Z.G. and Yu, X.* (2015) A novel Wnt5a-Frizzled4 signaling pathway mediates activity-independent dendrite morphogenesis via the distal PDZ motif of Frizzled 4. Dev. Neurobiol. 75(8):805-822.
12. Zheng J.J., Li S.J., Zhang X.D., Miao W.Y., Zhang D., Yao H. and Yu, X.* (2014) Oxytocin mediates early experience–dependent cross-modal plasticity in the sensory cortices. Nat. Neurosci. 17(3):391-399 [highlighted by same issue News and Views 17(3), 340 and by Nat. Rev. Neurosci. 15(3):139; selected as “exceptional” by Faculty 1000]
13. Peng Y.R., Hou Z.H. and Yu X.* (2013) The kinase activity of EphA4 mediates homeostatic scaling-down of synaptic strength via activation of Cdk5. Neuropharmacology 65(1):232-243.
14. Hou Z.H. and Yu X.* (2013) Activity-regulated somatostatin expression reduces dendritic spine density and lowers excitatory synaptic transmission via post-synaptic somatostatin receptor 4. J. Biol. Chem. 288(4):2501-2509.
15. Xu X.*, Xu Q., Zhang Y., Zhang X., Cheng T., Wu B., Ding Y., Lu P., Zheng J., Zhang M., Qiu Z., and Yu X.* (2012) A case report of Chinese brothers with inherited MECP2-containing duplication: autism and intellectual disability, but not seizures or respiratory infections. BMC Med Genet. 13(1):75 doi:10.1186/1471- 2350-13-75
16. Liu N., He S. and Yu X.* (2012) Early natural stimulation through environmental enrichment accelerates neuronal development in the mouse dentate gyrus. PLoS One 7(1):e30803. doi: 10.1371/journal.pone.0030803
17. Peng Y.R., Zeng S.Y., Song H.L., Li M.Y., Yamada M.K., and Yu X.* (2010) Postsynaptic spiking homeostatically induces cell-autonomous regulation of inhibitory inputs via retrograde signaling J. Neurosci. 30(48):16220-16231, cover story.
18. He S., Ma J., Liu N. and Yu, X.* (2010) Early enriched environment promotes neonatal GABAergic neurotransmission and accelerates synapse maturation. J. Neurosci. 30(23):7910-7916.
19. Tan Z.J., Peng Y., Song H.L. and Yu X.* (2010) N-cadherin dependent neuron-neuron interaction is required for the maintenance of activity-induced dendrite growth. Proc. Natl. Acad. Sci. USA 107(21):9873-9878, cover story.
20. Peng Y.R., He S., Marie H., Zeng S.Y., Ma J., Tan Z.J., Lee S., Malenka R.C.*, and Yu X.* (2009) Coordinated changes in dendritic arborization and synaptic strength during neural circuit development. Neuron 61(1):71-84. (Selected by Faculty 1000).
21. Yu, X.* and Malenka R.C.* (2004) Multiple functions for the cadherin/catenin complex during neuronal development. The Cytoskeleton and Synaptic Function Issue Neuropharm. 47(5):779-¬786.
22. Yu X.* and Malenka R.C.* (2003) β¬-catenin is critical for dendritic morphogenesis. Nature Neurosci. 6(11): 1169-¬1177, cover story.

Reviews and Editorials
1. Yu X.*, Qiu Z.* and Zhang D.* (2017) Recent Research Progress in Autism Spectrum Disorder. Neurosci. Bull. 33(2):125-129 (editorial)
2. Stoop R.* and Yu X.* (2017) Special issue on: “Oxytocin in development and plasticity”. Developmental Neurobiology 77(2):125-127 (editorial)
3. Yu X. (2011) Tools for studying the role of N-cadherin mediated extracellular interaction in neuronal development and function. Cell Adhesion & Migration 5(3):227-231
Teaching
Neural development and plasticity (Fall Semester, English)
Laboratory Introduction