PubMed search for Dr. Peng Jin

Areas of Specialization/Research Interests:
Non-coding RNAs in neural development and brain disorders
RNA-mediated neurodegeneration
Molecular basis of mental retardations
Epigenetic regulation in brain development

Education:
Ph.D., Molecular and Developmental Biology, University of Cincinnati College of Medicine and Cincinnati Children’s Hospital Research Foundation, Ohio, 1999
B.S., Molecular Biology, University of Science and Technology of China, P.R. China, 1994

Research Description:
The importance of non-coding RNAs has been increasingly recognized within the last several years, particularly with the identification of new classes of small RNAs, such as microRNAs (miRNAs). These non-coding RNAs play important roles in neural development and can be involved in neuronal translation control (miRNAs) or transcription regulation (small modulatory RNAs in the fate specification of adult neural stem cells), and can be pathogenic (non-coding repeats in neurodegeneration). The ultimate goal of my lab is to understand the roles of non-coding RNAs in neural development and the pathogenesis of brain disorders. Currently we are focusing on three areas: 1) the role of microRNA pathways in learning and memory; 2) the molecular basis of RNA-mediated neurodegeneration; and 3) the role of small non-coding RNAs in epigenetic regulation.

The role of the microRNA pathway in mental retardation: Fragile X syndrome, a common form of inherited mental retardation, is caused by the loss of fragile X mental retardation protein (FMRP). FMRP is an RNA-binding protein that shuttles between the nucleus and cytoplasm. FMRP has been implicated in protein translation, and is proposed to be involved in the local regulation of protein synthesis at synapses. However, the mechanism regulating synaptic translation is poorly understood. Our recent works have led to the identification of mRNA ligands of FMRP, and demonstrated the biochemical and genetic interaction between FMRP and the microRNA pathway. Currently we are trying to understand how FMRP utilizes the microRNA pathway to regulate the translation of its mRNA targets.

The molecular basis of RNA-mediated neurodegeneration: Very recently, a novel progressive neurodegenerative disorder has been recognized in fragile X premutation carriers, where FMRP is expressed but the mRNA contains elongated non-coding CGG repeats. Strikingly, no evidence of neurodegeneration has been found in either fragile X patients or in the Fmrl knockout mouse model, indicating that modulation of FMRP levels does not account for the neurodegeneration observed in these carriers. Using Drosophila as a model system, we have demonstrated that fragile X premutation rCGG repeats are indeed pathogenic and cause neurodegeneration. Using this fly model we are testing the model that through specific interaction with rCGG repeat-binding protein(s), fragile X premutation rCGG repeats interfere with specific pathway(s) and cause neuronal cell death/neurodegeneration.

The role of small non-coding RNAs in epigenetic regulation:Recent studies suggest that small non-coding RNAs could be used to target repressive chromosomal complexes to specific chromosomal loci. In this novel process, RNA provides specificity for the precise targeting of silent chromatin complexes to particular genomic loci. Also it was discovered that small non-coding RNAs could function in activating gene expression. We are interested in understanding the role of small non-coding RNAs in epigenetic modulation.

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Selected Publications:
Brown, V.*, Jin, P.* (equal contribution), Ceman, S., Darnell, J. C., O'Donnell, W. T., Tenenbaum, S. A., Jin, X., Feng, Y., Wilkinson, K. D., Keene, J. D., Darnell, R. B., and Warren, S. T. (2001). Microarray identification of FMRP-associated brain mRNAs and altered mRNA translational profiles in fragile X syndrome. Cell 107, 477-87.

Darnell, J. C., Jensen, K. B., Jin, P., Brown, V., Warren, S. T., and Darnell, R. B. (2001). Fragile X mental retardation protein targets G quartet mRNAs important for neuronal function. Cell 107, 489-99.

Jin, P., Zarnescu, D.C., Zhang, F., Pearson, C.E., Lucchesi, J.C., Moses, K and Warren, S.T. (2003). RNA-mediated neurodegeneration caused by the fragile X premutation rCGG repeats in Drosophila. Neuron, 39, 739-747.

Jin, P., Zarnescu, D.C., Ceman, S., Nakamoto, M., Mowrey, J., Jongens, T.A., Nelson, D.L., Moses, K., and Warren, S.T. (2004). Biochemical and genetic interaction between the fragile X mental retardation protein and the microRNA pathway. Nature Neuroscience, 7, 113-117.

Jin, P., Alisch, R.S. and Warren, S.T. (2004). RNA and microRNAs in fragile X mental retardation. Nature Cell Biology 6, 1048-1053.

Zarnescu, D.C., Jin, P., Nakamoto, M., Dockendorff, T.C., Feng, Y., Jongens, T.A., Warren, S.T., and Moses, K. (2005). Fragile X and Lgl proteins form a functional complex in fly and mouse neural development. Development Cell, 8, 43-52 (Cover).