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faculty profile |
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Research Description:
The Myc oncoprotein is a transcriptional activator and repressor whose function is essential for normal development. Mice lacking functional myc genes die early in embryogenesis. As an oncoprotein, however, an excess of Myc protein induces tumor formation, and is present in ~80% of human tumors. Myc is capable of binding to 10% of all genes in the mammalian genome, and it is unclear how a developing embryo limits the DNA binding of its abundant Myc proteins in order to avoid Myc's potential for inducing tumorigenesis. My lab examines the genome-wide control of Myc activity in the Drosophila embryo. We have discovered several nuclear, chromatin remodeling proteins that are involved in Myc's ability to both activate and repress its targets (Polycomb, Ash1, Pho). These proteins have well-known roles in cell fate specification, and we are interested in understanding the mechanism by which these proteins, and others, control Myc activity throughout embryogenesis. |
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Recent Publications:
J.M. Goodliffe, Eric Wieschaus. Indirect mircroarray targets of Myc and Pc: A Molecular View of Epistasis. In preparation.
J.M. Goodliffe, M. Cole, E. Wieschaus (2007). Coordinated Regulation of Myc Trans-activation Targets by Polycomb and the Trithorax Group Protein Ash1. BMC Molecular Biology, 8:40.
M. Beaucher*, J.M. Goodliffe*, E. Hersperger, S. Trunova, H. Frydman, A. Shearn (2007). Drosophila brain tumor metastases express both neuronal and glial cell type markers. Developmental Biology, 301(1):287-97. *Authors contributed equally.
J.M. Goodliffe, E. Wieschaus, M. Cole (2005). Polycomb mediates Myc autorepression and its transcriptional control of many loci in Drosophila. Genes & Development, 19(24):2941-2946.
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