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Education / Training
Princeton University, Department of Molecular Biology. Postdoctoral research with Drs.
Eric Wieschaus and
Michael Cole, 2001-2006.
Johns Hopkins University, Department of Biology. PhD, 2001.
Carnegie Mellon University, B.S. in Biology, 1995.
Research Interests
Overview: Molecular genetics and genomics of cancer
Excessive accumulation of the
Myc oncoprotein leads to tumorigenesis and is present in 50% of all human tumors. Myc
is a DNA-binding protein that is able to both activate and repress transcription of many genes, and is capable of binding to over
10% of all genes in the human genome. While Myc induces dramatic changes in expression in vivo, Myc is a weak transcriptional activator in vitro, and repression by Myc does not clearly require Myc binding to DNA.
My lab is interested in understanding how Myc induces such dramatic changes in gene expression, especially during embryogenesis when Myc levels are normally high. We use the
Drosophila embryo for our work, which allows us to rapidly obtain thousands of genetically manipulated embryos for our experiments. 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, affect Myc activity in different cell types and in general.
Transcriptional activation and repression by Myc in the Drosophila embryo
Ectopic Myc in the Drosophila embryo increases expression of many genes (red) and decreases expression of many genes (green). Genes whose levels rise or fall with ectopic Myc change during embryonic development, and we study this developmental control of a genome's response to ectopic Myc. Chromatin structure, sequence elements and modifier proteins are all potential mediators of the response to Myc, as they are for all transcription factors. We use genetic, genomic and molecular biological tools to address the question of what controls a genome's response to Myc.
Lab Members
Abid Khan, PhD student
Kaveh Daneshvar, PhD student
Sam Vaughan, MA student
Amy Lee, post-bac
Alaleh Khademi, undergraduate
Wes Shover, Biology honors undergraduate
Olivia Santoso, Biology honors undergraduate
Courses
Biology 3166, Genetics. Spring semesters.
Molecular Mechanisms in Epigenetics. Fall semesters. Biology graduate students only.
Recent Publications
Abid Khan, Wesley Shover, Julie M. Goodliffe. 2009. Su(z)2 Antagonizes Auto-Repression by Myc in Drosophila, Increasing Myc Levels and Subsequent Trans-Activation. 2009. PLoS ONE. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0005076
Julie M. Goodliffe, Michael Cole and Eric Wieschaus. 2007. Coordinated Regulation of Myc Trans-activation Targets by Polycomb and the Trithorax Group Protein Ash1.
BMC
Molecular Biology,
8:40.
Michelle Beaucher*, Julie Goodliffe*, Evelyn Hersperger, Svetlana Trunova, Horacio Frydman and Allen Shearn. 2007. Drosophila brain tumor metastases express both neuronal and glial cell type markers. Developmental Biology, Jan 1;301(1) 287-97. *Authors contributed equally.
Julie M. Goodliffe, Eric Wieschaus and Michael Cole. 2005. Polycomb mediates Myc autorepression and its transcriptional control of many loci in Drosophila. Genes & Development,
2005 Dec 15;19(24) 2941.
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