Dr. Voss is an Assistant Professor in the Department of Biology at Middle Tennessee State University. She is committed to understanding what causes single ventricle and other congenital heart diseases, with the goal of translating basic science discoveries into therapies. She brings broad expertise in cardiogenesis, molecular biology, cutting-edge imaging, advanced genome-wide profiling and sequencing techniques. This foundation was developed during her postdoctoral training in the laboratory of Dr. Jonathan Epstein at the University of Pennsylvania and her PhD dissertation under Drs. Russell Norris and Joshua Lipschutz at the Medical University of South Carolina.

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Normal heart development requires precise timing of gene expression and silencing. When this balance is disrupted, heart cells can no longer grow and function properly. Many single gene mutations are known to cause congenital heart disease (CHD); however, over half of CHD cases have no known cause. Complex CHDs, such as single ventricle diseases (SVDs), likely arise from multiple gene disruptions that affect different heart cell populations in different ways. Understanding how gene expression is regulated is therefore key to understanding how its disruption leads to SVD.

One way that many genes can be perturbed at once is through disruption of epigenetic enzymes. These enzymes modify DNA or the histones that DNA is wrapped around, which controls whether genes are accessible for transcription. Because they can regulate the expression of many genes without changing the DNA sequence, epigenetic enzymes are exciting targets for SVD research.

The Voss Lab studies how two histone methylation enzymes, GLP and G9a, contribute to heart development. Mutations in these enzymes are linked to Kleefstra syndrome, a rare congenital disorder, and to several cancers. Kleefstra syndrome carries a high incidence of CHD, including complex defects such as double outlet right ventricle (DORV) and Tetralogy of Fallot, and SVDs such as hypoplastic left heart syndrome. In her postdoctoral work, Dr. Voss showed that loss of GLP and G9a in neural crest cells, a cell type that contributes to cardiac outflow tract development, not only disrupted gene expression but also caused heart defects such as DORV in mice. We are now identifying the genes that GLP and G9a directly regulate in neural crest cells and determining how their loss affects cardiomyocyte development. Our goal is to define the mechanisms underlying SVD development and to identify pathways from our mouse studies that could guide therapy development.

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