The Jun Yang Laboratory
Retinal degeneration is a group of conditions with vision loss mainly caused by photoreceptor cell death and retinal pigment epithelium malfunction. It generally includes retinitis pigmentosa and macular degeneration. These are hereditary diseases affecting millions of people in the world. Although many genes have been identified as responsible for these diseases, their physiological functions and pathogenic mechanisms are not clear. Additionally, many causative genes are still unidentified. Currently, no cures for these diseases are available.
The research in Dr. Yang’s laboratory is focused on the disease mechanisms and therapeutic treatments for retinal degenerative diseases using mouse models. Her research group investigates the biological functions of genes whose mutations are known to cause human retinal diseases. Using mouse models for these diseases, the group also studies how to treat these diseases by means of gene therapy. Dr.Yang’s team is also interested in the cell biology of photoreceptors, especially the cellular processes of intracellular trafficking, structural maintenance, and calcium regulation. The research led by Dr. Yang is attempting to understand more about retinal degenerative diseases, identify more candidate causative genes, and provide tactics to design various therapies.
The ongoing research projects in her laboratory are to understand three things: 1. how defects in the multiple protein complex at the periciliary ridge complex in photoreceptors cause retinal degeneration in Usher Syndrome type II, which is a disease with both vision and hearing loss; 2. the biological functions of the ciliary rootlet, a cytoskeletal structure, in photoreceptors and how its defects cause retinal degeneration; 3. how calcium homeostasis is maintained in photoreceptor synaptic terminals and whether it is involved in retinal degeneration. To address these questions, Dr. Yang’s laboratory uses a combination of experimental approaches including molecular biology, cell biology, biochemistry, and electrophysiology.
B.S., Nankai University, China
Ph.D., University of Massachusetts, Amherst, MA
Assistant Professor of Ophthalmology and Visual Sciences, University of Utah School of Medicine.
John A. Moran Eye Center
University of Utah School of Medicine
65 Mario Capecchi Drive
Bldg 523, S6160 JMEC
Salt Lake City, UT 84132
Tel: 801-213-2591 (office)
A sample of major publications from the Yang lab
Yang J, Liu X, Yue G, Adamian M, Bulgakov O and Li T. 2002 Rootletin, a novel coiled-coil protein, is a structural component of the ciliary rootlet. Journal of Cell Biology 159: 431-440.
Hong D, Pawlyk B, Sokolov M, Strissel KJ, Arshavsky VY, Yang J, Tulloch B, Wright AF and Li T. 2003 RPGR isoforms in photoreceptor connecting cilia and the transitional zone of motile cilia. Investigative Ophthalmology & Visual Science 44: 2413-2421.
Yang J, Gao J, Adamian M, Wen X, Pawlyk B, Zhang L, Sanderson MJ, Zuo J, Makino CL and Li T. 2005 The ciliary rootlet maintains long-term stability of the sensory cilia. Molecular and Cellular Biology 25: 4129-4137.
Yang J and Li T. 2005 The ciliary rootlet interacts with kinesin light chains and may provide a scaffold for kinesin-1 vesicular cargos. Experimental Cell Research 309: 379-389.
Yang J, Adamian M and Li T. 2006 Rootletin interacts with C-Nap1 and may function as a physical linker between the pair of centrioles/basal bodies in cells. Molecular Biology of the Cell, 17: 1033-1040.
Yang J and Li T. 2006 Rootletin. Experimental Eye Research, 83: 1-2.
Yang J, Pawlyk B, Wen X, Adamian M, Soloviev M, Michaud N, Zhao Y, Sandberg, MA, Makino CL and Li T. 2007 Mpp4 is required for proper localization of plasma membrane calcium ATPases and maintenance of calcium homeostasis at the rod photoreceptor synaptic terminals. Human Molecular Genetics, 16: 1017-1029.