Rong Liu, PhD

Assistant Professor

Organization:

West Virginia University School of Medicine

Department:

Biochemistry and Molecular Medicine

Classification:

Faculty

• BS, Shandong University, 2011
• PhD, Wayne State University School of Medicine, 2016

Wright M, Redford S, Vehar J, Courtney KC, Billington N & Liu R. MultiBac system-based purification and biophysical characterization of human myosin-7a. J Vis Exp. 2024 Aug 23: (210). PMID: 39248532

Holló A, Billington N, Takagi Y, Kengyel AM, Sellers JR & Liu R. Molecular regulatory mechanisms of human myosin-7a. J Biol Chem. 2023 Sep 8; 105243 PMID: 37690683

Hannaford MR, Liu R, Billington N, Swider ZT, Galletta BJ, Fagerstrom CJ, Combs C, Sellers JR, Rusan NM. Pericentrin interacts with kinesin-1 to drive centriole motility. J Cell Biol. 2022 Sep 5;221(9):e202112097

Liu R, Billington N, Yang Y, Bond C, Hong A, Siththanandan V, Takagi Y & Sellers JR. A binding protein regulates myosin-7a dimerization and actin bundle assembly. Nat Commun. Jan 25; 12(1): 563.

Nishimura Y, Shi S, Zhang F, Liu R, Takagi Y, Bershadsky AD, Viasnoff V & Sellers JR. The formin inhibitor, SMIFH2, inhibits members of the myosin superfamily. J Cell Sci. Feb 23: jcs.253708.

Lu W, Lakonishok M, Liu R, Billington N, Rich A, Glotzer M, Sellers JR & Gelfand VI. Competition between kinesin-1 and myosin-V defines Drosophila posterior determination. Elife Feb 14;9

Pal K, Nowak R, Billington N, Liu R, Ghosh A, Sellers JR & Fowler VM. Megakaryocyte migration defects due to nonmuscle myosin IIA mutations underly thrombocytopenia in MYH9-related disease. Blood May 21;135

Complete List of Publications

Cytoskeletal motors in neurosensory diseases and ciliopathies

Cytoskeletal motors are the engines of the cell, converting chemical energy into mechanical forces that power the movements essential for life. Our research focuses on an outstanding question in the field: how do cells harness and regulate the activity of these motors to support a wide range of biological functions? We explore this question in the context of neurosensory cells, which have highly specialized morphologies optimized for their roles in sensory transduction. We investigate how motor proteins contribute to the development of these distinctive cellular architectures and also how they mediate the sensory functions of these cells.

Myosin-7a in auditory function and disease

Auditory hair cells convert sound stimuli into neural signals. They achieve this through mechanotransduction, which occurs at the tips of specialized cellular protrusions called stereocilia. The motor protein myosin-7a plays key roles in the development and function of these stereocilia. Mutations in the myosin-7a gene (USH1B) are the leading genetic cause of Usher syndrome, the most common form of deaf-blindness in humans. The goal of our research is to understand how myosin-7a activity is regulated in stereociliary protein trafficking and mechanotransduction and to uncover the mechanisms behind Usher protein-related vision and hearing loss.

Kinesin-2 in ciliary trafficking and retinal ciliopathies

Cilia are microtubule-based cellular protrusions essential for sensing the external environment. In the retina, the outer segment (OS) of the photoreceptor cells is a specialized light-sensitive cilium responsible for transducing light into neural signals. Genetic defects in cilia cause a group of inherited conditions, known as ciliopathies, with clinical manifestations often including retinal dystrophy and blindness.

The assembly and function of cilia requires a sophisticated protein trafficking system, known as the intraflagellar transport (IFT) train. Kinesin-2 motors power the movement of this train to the tips of the cilia. Mutations in kinesin-2 are therefore linked to various types of ciliopathies including retinitis pigmentosa. Our research aims to uncover the molecular mechanism by which kinesin-2 powers the transport of the IFT train along cilia, how this is regulated, and how mutations disrupt this process, leading to ciliopathies and vision loss.

Kinesin-2 motors in neuronal transport

In additional to its role in ciliary transport, kinesin-2 also plays a role in transport within neurons. The requirements for transport in cilia and neurons are quite different due to the size differences between the two. We are investigating the mechanisms by which kinesin-2 is able to switch between transport in these two systems and the specializations it has acquired for functioning in each mode of transport.

Our approach

We employ a multidisciplinary approach that combines biophysics, biochemistry, and cell biology. We integrate high-resolution live-cell imaging with advanced single-molecule techniques to directly visualize motor protein dynamics both in vitro and in vivo. The bottom-up approach of building complex systems from their basic components provides a powerful system for understanding how motor proteins function. When coupled with a top-down approach of manipulating motor proteins in cells, this has enabled us to uncover novel mechanisms of myosins and kinesins across diverse biological processes, guiding our efforts to identify new therapeutic targets for motor-related human diseases such as deafness and blindness.

Link to the Lab Website

NIH R01 Rong Liu (PI) 12/2024 – 11/2029

Significance of Usher Protein Dynamics in Hair Cell Function and Deafness                             $ 2,182,205

This project aims to unravel the mechanisms behind the trafficking and assembly of Usher-1 interactome. the key molecular complex involved in the mechanotransduction process of auditory hair cells. Results are expected to provide critical insights into pathophysiology of Usher protein-related hearing loss, with the aim of identifying novel therapies for patients with Usher syndrome and other non-syndromic deafness.

NIH P20 Rong Liu (PPL) 01/2023 – 12/2024

Mechanistic Analysis of Kinesin-2 Motility and Its Regulation for Ciliary Trafficking              $228,000

This project aims to investigate the mechanisms by which kinesin-2 powers the anterograde transport within the cilia and the pathophysiology of its mutations in human patients that lead to ciliopathies.