Northwestern University Feinberg School of Medicine

Otolaryngology - Head and Neck Surgery

Auditory Molecular & Cell Biology Laboratory

Principal Investigator

Zheng

Jing Zheng, PhD, Associate Professor
jzh215@northwestern.edu
Website
NU Scholar profile

Areas of Research: Cell Biology, Hearing Sciences, Molecular Neuroscience

Current Research

The goal of my lab is to identify and investigate molecules that play important roles in mammalian hearing, thus to enrich our understanding of cochlear physiology, and to further develop a better strategy to prevent hearing loss. Our research has been centered on several important proteins expressed in cochlea.

Molecular Basis of Cochlear Amplification
Outer hair cells (OHCs) undergo rapid somatic length changes when the voltage across their membrane is altered. This unique somatic electromotility provides the local mechanical amplification of the cochlear response to sound. Without OHCs, the hearing threshold is elevated by 40-50 dB and frequency resolution deteriorates. Prestin is the motor protein of OHCs and it is required for cochlear amplification (Zheng et al., Nature, 2000). Coincidently, prestin is only expressed in OHCs, which are also the most vulnerable cells in the organ of Corti. We are investigating the connection between prestin’s function and the vulnerability of OHCs to a variety of ototoxic exposures including noise exposure. These studies will not only expand knowledge of prestin as the OHC-based cochlear amplifier at the molecular level, but also produce a deeper understanding of mechanisms associated with outer hair cells loss and synaptopathy.

Protein network of hair cells
We are focusing on several deafness-related proteins including CDH23, CEACAM16 and CAMSAP3. Cadherin 23 is a tip-link protein of hair cells. CEACAM16 is an adhesive protein localized at the tectorial membrane (TM) and serves to stabilize the tectorin-based matrix (Zheng e al. PNAS, 2011). CAMSAP3 is another newly identified microtubule minus-end binding protein that is expressed in the ear. Very often, genetic defects in a single protein can interfere with the entire network and cause deafness. We are in the process of investigating interactions among these proteins and their physiological roles for normal hearing and deafness.