Peter Jones Ph.D.: Biography/Education

Associate Professor; Mick Hitchcock Endowed Chair of Medical Biochemistry

Cellular and Molecular Pharmacology & Physiology | Department of Pharmacology

Education

  • Postdoc 2001, NICHD, NIH, Bethesda, MD; Epigenetics and Developmental Biology
  • Ph.D. 1997, Emory University, Atlanta, GA; Molecular Genetics
  • B.A. 1991, Miami University, Oxford, OH; Microbiology

Biography

Dr. Peter Jones has been investigating epigenetic mechanisms of gene regulation for most of his career and has been working on pathogenic mechanisms in facioscapulohumeral muscular dystrophy (FSHD) since 2003. As an undergraduate, an exciting research experience investigating ice-nucleating active bacteria with Dr. Marcia Lee turned his interests away from medical school and towards a career in biomedical research. Dr. Jones earned his PhD with Dr. Jeremy Boss at Emory University, working on gene regulation by primary immune response cytokines. His thesis work suggested a key role for enhancer chromatin structure in cytokine-mediated gene regulation. To further pursue the emerging role of chromatin as a regulatory mechanism, Dr. Jones did his post-doctoral fellowship at NIH with Dr. Alan P. Wolffe, one of the leaders in chromatin biology at the time. At NIH, Dr. Jones expanded his training into biochemistry and developmental biology, with a focus on epigenetics, DNA methylation, and chromatin remodeling. In 2001, Dr. Jones took a position as Assistant Professor at the University of Illinois at Urbana-Champaign and began identifying novel DNA methylation and chromatin remodeling complexes using Xenopus as a model system. When a graduate student introduced him to FSHD-an epigenetic disease-the lab began several exploratory projects and now works on FSHD translational research full-time. In 2008, Dr. Jones teamed up with his wife, Dr. Takako Jones, an expert in cell and developmental biology, and the two have been working as co-PIs ever since. The Jones lab has moved several times since UIUC, first joining the Boston Biomedical Research Institute, then the University of Massachusetts Medical School, and now the University of Nevada, Reno School of Medicine. Each institute has allowed us to develop new technologies and expertise for use in our FSHD research projects. Published studies from our lab utilize biochemistry, developmental biology, cell biology, genomics, and molecular biology approaches. Model systems include C. elegans, Xenopus laevis, honeybee, Drosophila, mouse, and primary mouse and human myogenic cells. The common theme of the lab continues to be exploring the epigenetics of muscle development and disease.

Research

Drs. Peter and Takako Jones function as co-PIs, combining expertise in gene regulation, biochemistry, and chromatin with expertise in cell, developmental, and molecular biology. Together we investigate epigenetic mechanisms of gene regulation, focusing on the combined roles of DNA methylation, histone post-translational modifications, active and repressive chromatin regulators, and noncoding RNAs.

We use a wide range of approaches, including biochemistry, cell biology, developmental biology, proteomics, and epigenomics, to investigate the epigenetic mechanisms that function during normal muscle development and establish and maintain disease states. Our experimental approaches have utilized several different model organisms including mouse, Drosophila, and primary human cell culture models and in vitro systems. Overall, we aim to design therapeutic approaches targeting the epigenetic regulatory mechanisms involved in human disease with a particular focus on myopathies. Our research covers three main areas:

Epigenetics of muscle development and disease

We use Facioscapulohumeral muscular dystrophy (FSHD) as a model to investigate epigenetic mechanisms of gene regulation. The genetic criteria for FSHD are merely disease permissive, with all forms of clinical FSHD exhibiting epigenetic dysregulation of the chromosome 4q35 D4Z4 macrosatellite array. The epigenetic mechanisms that go awry in FSHD include DNA methylation, histone post-translational modifications, Polycomb Group proteins, lncRNAs, RNA-dependent DNA methylation, and nuclear organization.

Engineering novel disease models for therapeutic development and preclinical testing

While we have used many animal models, including Drosophila and C. elegans, our lab is now focused on the design of human cellular and mouse models of FSHD for therapeutic development and pre-clinical testing. These models are based on aberrant expression of DUX4, a developmentally important gene that has been implicated in mediating FSHD pathophysiology. Our FSHD disease models are used to test small molecule, ncRNA, and CRISPR-based therapeutic approaches.

RNA-binding proteins involved in development and disease

We focus on two highly conserved proteins, FRG1 and MeCP2, which we have identified as RNA-binding proteins. In addition to interacting with select mRNAs, FRG1 is also an actin bundling protein critical for muscle development and a direct transcriptional target of the DUX4-FL transcription factor implicated in FSHD. MeCP2 is an epigenetic regulator critical for neuronal development and the gene most commonly mutated in Rett Syndrome.


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