Zizhen Wu, PhDAssistant Professor

Department of Neurobiology
Medical Research Building, Room 2.143D (O)/ 2.100 (L)
Route: 1069 | Tel: (409) 266-1659 | Lab: (409) 747-9003
 | ziwu@utmb.edu

Education and Training

Postdoctoral Fellow:  Johns Hopkins University School of Medicine and The Scripps Research Institute
Ph.D.: University of Texas Graduate School of Biomedical Science 


Research Interests

Living cells constantly sense and respond to mechanical stimuli arising from the outer world, neighboring cells and surrounding extracellular matrix by converting them into biochemical signals that trigger specific cellular responses. This process is termed mechanotransduction and is fundamental to hearing, touch, nociception, respiration, and proprioception. However, the molecules that mediate/regulate mechanotransduction are poorly defined. Thus, identifying molecules underlying mechanotransduction in mechanosensory cells, uncovering their modulating mechanisms, and describing their roles in various diseases/symptoms are the primary foci of sensory biology studies, which hold the promise to understand sensory processing and uncover novel strategies for mechanosensory disorders.

My long-term research goals involve the development of a comprehensive understanding of the molecular mechanisms of sensory perception and related disorders in order to develop new methods for treatment. In the near future, I will identify molecules underlying/modulating mechanotransduction in sensory neurons and define the mechanisms underlying the plasticity of mechanotransduction in various diseases/symptoms, including deafness and mechanical pain.



Selected Publications:

Wu Z*, Li L, Li G, Xu G, and Yang Q*. Decreasing neuronal excitability by targeting KCNQ channels improves neurobehavioral function after spinal cord injury.  J Pharmacol Exp Ther., 2020; 373: 72-80 * Co-corresponding author

Cunningham C, Qiu X, Wu Z, Zhao B, Peng G, Kim YH, Lauer A, and Müller U. TMIE defines pore and gating properties of the mechanotransduction channel of mammalian cochlear hair cells. Neuron, 2020; 107: 126-143

Cunningham C, Wu Z, Jafari A, Zhao B, Schrode K, Harkins-Perry S, Lauer A, Mueller U. The murine catecholamine methyltransferase mTOMT is essential for mechanotransduction by cochlear hair cells. Elife, 2017; e24318

Wu Z, Grillet N, Zhao B, Cunningham C, Harkins-Perry S, Coste B, Ranade S, Zebarjadi N, Beurg M, Fettiplace R, Patapoutian A, Müller U. Mechanosensory hair cells express two molecularly distinct mechanotransduction channels. Nat. Neurosci., 2017; 20: 24-33

Zhao B, Wu Z, Müller U. Murine Fam65b forms ring-like structures at the base of stereocilia critical for mechanosensory hair cell function. Elife, 2016; 5: e14222. PMCID: PMC4898930

Zhao B, Wu Z, Grillet N, Yan L, Xiong W, Harkins-Perry S, Müller U. TMIE is an essential component of the mechanotransduction machinery of cochlear hair cells. Neuron. 2014; 84: 954-967. PMCID: PMC4258123

Yang Q, Wu Z, Hadden JK, Odem MA, Zuo Y, Crook RJ, Frost JA, Walters ET. Persistent pain after spinal cord injury is maintained by primary afferent activity. J. Neurosci. 2014; 34: 10765-10769. PMCID: PMC4122805

Wu Z, Yang Q, Crook RJ, O'Neil RG, Walters ET. TRPV1 channels make major contributions to behavioral hypersensitivity and spontaneous activity in nociceptors after spinal cord injury. Pain. 2013; 154: 2130-2141.