Dr. Gulick studies regulated expression & functions of MEF2 alternative splicing (AS) variants & concerted AS programs in energy metabolism.
Dr. Gulick is a graduate of University of Rochester School of Medicine.
View All Publications
Nuclear respiratory factor 1 controls myocyte enhancer factor 2A transcription to provide a mechanism for coordinate expression of respiratory chain subunits.
Ramachandran B, Yu G, Gulick T
J Biol Chem. 2008 May 2;283(18):11935-46
Myocyte enhancer factor 2A is transcriptionally autoregulated.
Ramachandran B, Yu G, Li S, Zhu B, Gulick T
J Biol Chem. 2008 Apr 18;283(16):10318-29
Processing body autoantibodies reconsidered.
Bloch DB, Gulick T, Bloch KD, Yang WH
RNA. 2006 May;12(5):707-9
Alternative pre-mRNA splicing governs expression of a conserved acidic transactivation domain in myocyte enhancer factor 2 factors of striated muscle and brain.
Zhu B, Ramachandran B, Gulick T
J Biol Chem. 2005 Aug 5;280(31):28749-60
Phosphorylation and alternative pre-mRNA splicing converge to regulate myocyte enhancer factor 2C activity.
Zhu B, Gulick T
Mol Cell Biol. 2004 Sep;24(18):8264-75
Tod Gulick's Research Focus
Type 2 Diabetes, Cardiomyopathies, Heart Disease, Diabetes - General, Cardiovascular Diseases
Our lab studies the regulated expression of the myocyte enhancer factor 2 (Mef2) genes at levels of transcription and alternative splicing, and the selective functions of encoded Mef2 transcription factor isoforms. We have developed tools for functional genomic screens of isoform-selective protein and genetic interactions, and are developing mouse models to determine corresponding roles in vivo. We are also examining networks of alternative splicing involved in the regulation of fuel metabolism in striated muscle.
Tod Gulick's Research Report
Mef2 factors are master regulators of myogenesis and are the only transcription factors that direct the establishment of all three types of muscle (cardiac, skeletal, smooth). Mef2s also control genetic programs governing skeletal muscle fiber type, physiological and pathological cardiac hypertrophy, and fuel metabolic pathways in striated muscle. Genetic models have established that Mef2s also play pivotal roles in neuron differentiation, survival and synapse formation, T and B lymphocyte activation, and bone development. There are four Mef2 paralogs in vertebrates. The paralogs have similar patterns of alternative splicing that ramify on encoded protein structures and both the regulated alternative splicing and the encoded alternative Mef2 domains are conserved across paralogs and across evolution. We are exploring the functions of the Mef2-splicing isoforms using biochemical and molecular biological approaches in cell-based and mouse models. It is now apparent that the primary transcripts of more than 90 percent of human genes are alternatively spliced. Many of these events result in the generation of protein isoforms or the production of processed transcripts that are subject to nonsense mediated decay. We are addressing the hypothesis that there are master regulators of alternative splicing that influence fuel metabolism, superimposing a level of control onto that given by substrate availability, hormonal signaling, allosteric control and transcriptional regulation. Because skeletal muscle is second only to brain in the richness of alternative splicing, and fuel utilization is highly regulated in this tissue, we are using next-generation sequencing of muscle RNA and computational biological approaches to explore networks of alternative splicing that impact fuel utilization.
About Tod Gulick
Tod Gulick, M.D., is a graduate of Bowdoin College (B.A, liberal arts/physics) and the University of Rochester School of Medicine (M.D.). He completed his Internal Medicine internship and residency at Barnes Hospital, Washington University School of Medicine, in St. Louis, MO, followed by post-doctoral research fellowships in the Departments of Pharmacology and Medicine at Washington University School of Medicine, the Department of Molecular Biology, Massachusetts General Hospital, Boston, and the Genetics Department, Harvard Medical School, Boston, MA. Before joining Sanford-Burnham, Dr. Gulick was a member of the Diabetes Unit in the Department of Medicine at Massachusetts General Hospital and an Assistant Professor of Medicine at Harvard Medical School.
Honors and Recognition
Surdna Foundation Fellowship in Physics, Bowdoin College
Fellowship, Radiation Effects Research Foundation, Hiroshima, Japan
F32 Individual National Research Service Award, NIGMS
Capps Scholarship in Diabetes, Harvard Medical School
K02 Independent Scientist Career Development Award, NIDDK
Basil O’Connor Scholar, March of Dimes Birth Defects Foundation.