Vanderbilt University School of Medicine

Murdock, Deborah G. , Ph.D.
Research Assistant Professor of Molecular Physiology and Biophysics

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Phone Number: 2-6325


Murdock, Deborah's picture

Office Address   Mailing Address

525D Light Hall

525D Light Hall 0615

Research Keywords
mitochondrial biogenesis, mitochondrial genetics, mtDNA, aging, microarrays, mice, transcription, nuclear hormone receptors, oxidative stress, energy regulation, metabolism, muscle,Gene regulation

Research Specialty
Mitochondrial biogenesis, coordinate control of mitchondrial and nuclear genomes, non-mendelian genetics

Research Description
Mitochondria are extremely dynamic organelles that are capable of proliferation in response to increased energy demand or environmental temperature. It has been estimated that approximately 3000 genes are required to create a functional mitochondrion, including the 13 genes that reside in the mitochondrial DNA. Therefore, the response to a signal to proliferate mitochondria must require the orchestrated coordination of two genomes, the nuclear and the mitochondrial. The control of mitochondrial respiration is important in metabolic regulation, and for humans as it relates to obesity, diabetes, cancer, heart disease, and genetic metabolic defects. My main research interest is in mitochondrial biogenesis; in particular, how the cell responds to a deficiency of energy, what the nature of this signal is, and how it is translated into mitochondrial proliferation. Current projects include investigation of putative mitochondrial biogenesis genes identified by microarray analysis of the transcriptional profile of a mouse model of mitochondrial disease.

Energy deficient skeletal muscle from adenine nucleotide translocator (ANT1) deficient mice exhibit dramatic proliferation of mitochondria. Identification of genes up-regulated in the muscle of these genetically engineered mice has identified both nuclear and mitochondrial genes involved in energy production, and should identify elements important for mitochondrial proliferation. The product of one gene found to be transcriptionally up-regulated in ANT1-deficient skeletal muscle was first identified as a protein interacting with PPAR??, a nuclear hormone receptor type transcription factor known to be important in energy regulation. When overexpressed in yeast, this gene has been shown to cause mitochondrial proliferation. Some of the current work in my laboratory consists of evaluating the results of the regulated overexpression of this gene in cultured cells.
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Boczko, EM, Cooper, TG, Gedeon, T, Mischaikow, K, Murdock, DG, Pratap, S, Wells, KS. Structure theorems and the dynamics of nitrogen catabolite repression in yeast. Proc Natl Acad Sci U S A, 102(16), 5647-52, 2005. PMCID:556013

Postdoctoral Position Available

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