Xuanmao Chen

ASSISTANT PROFESSOR
Phone: (603) 862-4542
Office: Molecular, Cellular, & Biomedical Sciences, Rudman Hall Rm 389, Durham, NH 03824
Xuanmao Chen

We are interested in revealing the mysteries of primary cilium. Primary cilium is a tiny, hair-like, microtubule-based organelle present in almost every vertebrate cell. The microenvironment in cilium is unique compared to most other actin-based signaling domains. It is highly sensitive to extracellular signals such as nutrients, morphogens, hormones, and mechanical stimuli. Cilium emanates from the basal body residing underneath the plasma membrane. Dismantling primary cilium is a prerequisite for the initiation of cell cycle. The primary cilium is thus considered the “keeper of the key for cell division”. Primary cilium plays crucial roles in a variety of physiological functions including cell division, development, sensory perception and energy balance. Defect of cilia lead to a broad spectrum of human diseases including polycystic kidney disease, obesity, cancer, diabetes, sensory defects and intellectual disability. In the nervous system, every neuron virtually has one primary cilium. Neuronal primary cilium is a unique type of neuronal process, locating in the cell boy but lacking synaptic structures or connections. Therefore, neuronal primary cilium mostly depends on metabotropic receptors to transmit signals downstream. A couple of GPCRs such as type 3 somatostatin receptor and type 6 serotonin receptor are highly expressed in primary cilium. Type III adenylyl cyclase (AC3) is a predominant adenylyl cyclase and enriched in neuronal primary cilium. In this regard, AC3 is a key enzyme for cAMP-mediated signaling in neuronal cilium and is a crucial element for the “antenna” to execute its functions in neuron.

We are dedicated to studying the cAMP signaling specifically in primary cilia. First, our lab aims to determine how type III adenylyl cyclase (AC3) at neuronal primary cilia affects neuronal function and examine how defects of AC3 lead to major depression and obesity. We are also interested in unraveling the contributions of primary cilia in neurodegeneration and brain aging.

We have a couple of research opportunities for undergraduates and graduates to acquire research expertise in primary cilia and skills in the field of neuroscience. We also have one open postdoctoral position to study the cAMP signaling in primary cilia. The research approaches include electrophysiology and EEG/EMG recording, mouse behavioral analysis, in vivo imaging using fiber-optic endoscope, molecular and cellular tools. We are establishing collaborations with research labs in USA, Germany, and Canada. Interested individuals (for the postdoc position) should have a Ph.D and research experience in neurobiology, and/or cell biology. Interested candidates at various levels are encouraged to contact Dr. Xuanmao Chen at Xuanmao.Chen@unh.edu

Education

  • Ph.D., Physiology, University of Tuebingen
  • M.S., Genetics, Fudan University
  • B.S., Biology, Nanchang University

Courses Taught

  • BCHM 860: Pharmacology
  • BCHM 999: Doctoral Research
  • BIOL 411: Honors/Intro Biol:Mol/Cellular
  • GEN 999: Doctoral Research
  • INCO 590: Rsrch Exp/MCBS
  • INCO 790: Rsrch Exp/MCBS
  • MCBS 999: Doctoral Thesis

Selected Publications

Sterpka, A., & Chen, X. (2018). Neuronal and astrocytic primary cilia in the mature brain. Pharmacological Research, 137, 114-121. doi:10.1016/j.phrs.2018.10.002

Chen, X., Luo, J., Leng, Y., Yang, Y., Zweifel, L. S., Palmiter, R. D., & Storm, D. R. (2016). Ablation of Type III Adenylyl Cyclase in Mice Causes Reduced Neuronal Activity, Altered Sleep Pattern, and Depression-like Phenotypes. Biological Psychiatry, 80(11), 836-848. doi:10.1016/j.biopsych.2015.12.012

Challis, R. C., Tian, H., Wang, J., He, J., Jiang, J., Chen, X., . . . Ma, M. (2015). An Olfactory Cilia Pattern in the Mammalian Nose Ensures High Sensitivity to Odors. Current Biology, 25(19), 2503-2512. doi:10.1016/j.cub.2015.07.065

Chen, X., Cao, H., Saraf, A., Zweifel, L. S., & Storm, D. R. (2015). Overexpression of the Type 1 Adenylyl Cyclase in the Forebrain Leads to Deficits of Behavioral Inhibition. Journal of Neuroscience, 35(1), 339-351. doi:10.1523/jneurosci.2478-14.2015

Wardlaw, S. M., Phan, T. X., Saraf, A., Chen, X., & Storm, D. R. (2014). Genetic disruption of the core circadian clock impairs hippocampus-dependent memory. Learning & Memory, 21(8), 417-423. doi:10.1101/lm.035451.114

Chen, X., Qiu, L., Li, M., Dürrnagel, S., Orser, B. A., Xiong, Z. -G., & MacDonald, J. F. (2010). Diarylamidines: High potency inhibitors of acid-sensing ion channels. Neuropharmacology, 58(7), 1045-1053. doi:10.1016/j.neuropharm.2010.01.011

Paukert, M., Chen, X., Polleichtner, G., Schindelin, H., & Gründer, S. (2008). Candidate Amino Acids Involved in H+Gating of Acid-sensing Ion Channel 1a. Journal of Biological Chemistry, 283(1), 572-581. doi:10.1074/jbc.m706811200

Chen, X., & Gründer, S. (2007). Permeating protons contribute to tachyphylaxis of the acid-sensing ion channel (ASIC) 1a. The Journal of Physiology, 579(3), 657-670. doi:10.1113/jphysiol.2006.120733

Chen, X., Kalbacher, H., & Gründer, S. (2006). Interaction of Acid-sensing Ion Channel (ASIC) 1 with the Tarantula Toxin Psalmotoxin 1 is State Dependent. The Journal of General Physiology, 127(3), 267-276. doi:10.1085/jgp.200509409

Chen, X., Kalbacher, H., & Gründer, S. (2005). The Tarantula Toxin Psalmotoxin 1 Inhibits Acid-sensing Ion Channel (ASIC) 1a by Increasing Its Apparent H+Affinity. The Journal of General Physiology, 126(1), 71-79. doi:10.1085/jgp.200509303

Most Cited Publications