The Interdisciplinary Biomedical Sciences Ph.D. Program

Big enough to be on the forefront of research

Small enough for one on one interactions with experts

We foster a cooperative climate for training and research that has an established record of timely graduations and alumni successes.  We also provide competitive stipends in a vibrant region with a low cost of living.

Featured Program Faculty, Yong-jie Xu Laboratory

The Xu lab studies the checkpoint mechanism that coordinates DNA replication with cell cycle progression. Various factors such as DNA damage and polymerase toxins can block DNA replication, which activates the checkpoint to slow down mitosis so that the cells can have enough time to properly finish the DNA synthesis before cell division. Progress in this research will advance our knowledge of the mechanisms that control cell proliferation and prevent oncogenesis. His lab also studies therapeutics identified from basic research for better treatment of cancer or infectious diseases.

Integrative Biology and Toxicology

Are you interested in studying the mammalian organism as an entire system or investigating a specific organ system as a part of the whole organism? If so, consider the Integrative Biology and Toxicology area of concentration.

Molecular Genetics and Cell Biology

Research training opportunities in the Molecular Genetics and Cell Biology area of concentration extend across the molecular, cellular, intercellular and organismal levels of biology.


Neuroscience and Physiology

The Neuroscience and Physiology area of concentration involves investigating the function of the cell, the organ and the whole animal, using molecular, cellular, physiological and behavioral approaches.

Structural and Quantitative Biology

Traditional biological research and computational science methods have come together to form the next wave in research. This combination is maximized in the Structural and Quantitative Biology area of concentration.

Research Spotlight

Huntingtin gene. As a result, the disease symptoms are caused by some combination of the mutated huntingtin protein, toxic huntingtin RNA, and the extra glutamines encoded by the CAG repeats. Most studies of HD have focused on the central nervous system and the motor defects are widely considered to be the result of neurodegeneration. The laboratory of Dr. Andrew Voss in the Wright State University Department of Biological Sciences has hypothesized that defects caused by the huntingtin gene in skeletal muscle may cause some of the motor symptoms of HD.  

In a recent study published in The Journal of General Physiology , researchers at Wright State University and the California State Polytechnic University in Pomona (Cal Poly Pomona) found that muscle maturation is disrupted in the mouse model of HD. A Commentary published in the same issue of the journal provides a more general description of the research. Members of the Voss lab at Wright State who co-authored this paper include the first author, Daniel Miranda (student in Biomedical Sciences PhD Program) and Dr. Shannon H. Romer. Additionally, Dr. Volker Bahn from the Biological Sciences Department is an author on the paper. The results of the study points to an early and progressive disease of muscle tissue that may develop independent of neurodegeneration, which could lead to therapies targeting skeletal muscle to improve patients' motor function according to Voss. "Our results support the idea that HD is a myopathy as well as a neurodegenerative disease and may provide a new opportunity to improve patient care by targeting skeletal muscle tissue," Voss says. In addition, researchers and clinicians may be able to use the skeletal muscle defects as biomarkers to track the progress of HD, a much easier task than examining patients' brain tissue.

Photo of Andrew Voss, Ph.D.This study extended previous work led by Voss while he was at Cal Poly, in which he and colleagues examined late-stage HD mice. The initial focus of the recent work was to compare HD mice with the healthy, wild-type mice (the control group) throughout the course of the disease. They found a progressive reduction in function of a protein called ClC-1 that carries chloride ions into and out of the cells. The disruption in ClC-1 proteins was linked to the disease-causing CAG repeats via problems in mRNA processing. The team found that the defects in ClC-1 function and mRNA processing began before the motor symptoms appeared. Surprisingly, the mRNA encoding ClC-1 was misprocessed in both HD and control mice when they were young, but, as they grew older, only healthy animals were able to start correctly processing the RNA to produce functional ClC-1. This suggested that skeletal muscle maturation was disrupted in the HD mice. They confirmed this by showing that mouse models of juvenile- and adult-onset HD expressed a form of myosin that is normally only found in embryonic and neonatal mice.

Clinically, the early and progressive defects in muscle ClC-1 mRNA processing could be used as a much needed biomarker to assess disease progression in regular HD patients and those receiving test therapeutics. The needle biopsy required to assess mRNA processing in skeletal muscle would be much easier than the current monitoring procedures that involves the use of MRI and PET scans. Additionally, the work reveals novel therapeutic targets for the motor symptoms.


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