Dan Savic

grad student

bioI received a bachelor’s degree at the University of Milwaukee-Wisconsin in Microbiology/Molecular Biology.

As an undergraduate, I worked in various laboratories at the Medical College of Wisconsin. I initially started as a volunteer research assistant performing in vivo physiological studies in rats under the mentorship of Dr. Timothy Lowry in the Department of Physiology. This entailed measuring heart rate, blood pressure and brain oxygen levels in neonatal and adult rats during hypoxia.

Following this, I became a research technician in the laboratory of Dr. Michael Olivier at the Human and Molecular Genetics Center (HMGC) at the Medical College of Wisconsin where I initially worked on genotyping SNPs around candidate genes for obesity and other metabolic phenotypes.

In addition, during this period I was a SPUR (Summer Program for Undergraduate Research) student at the Medical College of Wisconsin for two summers.

Upon completion of my undergraduate degree, I continued to work in the Olivier lab as a full-time technician. Subsequent projects centered on proteomics research. I worked on developing novel proteomic technologies including a protein array that would be used in conjunction with mass spectrometry to identify changes in the cellular proteome.

Projects

projectGenome wide association studies have consistently implicated non-coding variation within the TCF7L2 locus with type 2 diabetes (T2D) risk. While this locus represents the strongest genetic determinant for T2D risk in humans, it remains unclear how these non-coding variants affect disease etiology. However, recent studies have highlighted the importance of cis-regulatory variation in non-coding intervals in affecting risk to common diseases.

One goal of my project is to characterize the TCF7L2 regulatory landscape using in vivo mouse transgenic reporter assays in hopes of uncovering candidate disease-risk enhancers and as corollary, potential disease mechanisms.

To further determine whether variation in Tcf7l2 expression results in altered glucose metabolism and therefore diabetes susceptibility, I have been developing and phenotyping mouse models to characterize the effects of Tcf7l2 ablation and over-expression on glucose homeostasis and T2D risk.

Publications

Savic D, Bell GI, Nobrega MA (2012) An in vivo cis-regulatory screen at the type 2 diabetes associated TCF7L2 locus identifies multiple tissue-specific enhancers. PLoS One 7(5) e36501 PMID:22590553

Sakabe NJ, Savic D, Nobrega MA (2012) Transcriptional enhancers in development and disease. Genome Biol 13(1) 238 PMID:22269347

Savic D, Ye H, Aneas I, Park SY, Bell GI, Nobrega MA (2011) Alterations in TCF7L2 expression define its role as a key regulator of glucose metabolism. Genome Res 21(9) 1417-25 PMID:21673050