William C. Copeland, Ph.D.

Biochemist and discover of the human POLG gene, William Copeland is a Senior Investigator at the National Institutes of Health, the National Institutes of Environmental Health Sciences (NIEHS) and has been studying POLG and mitochondrial DNA replication for more than 30 years.

William Copeland received his Ph.D. in chemistry/biochemistry from the University of Texas at Austin studying structure-function relationships in proteins. He then completed a postdoctoral fellowship at Stanford University School of Medicine studying nuclear DNA polymerases. In 1993, he joined the National Institutes of Environmental Health Sciences, NIH, in Research Triangle Park, NC and is currently the head of the Mitochondrial DNA Replication Group in the Genome Integrity and Structural Biology Laboratory within the Intramural Research Division and Deputy Chief of the Genome Integrity and Structural Biology after serving as Chief for 14 yrs. Dr. Copeland has previously served as president of the Mitochondrion Research Society, and has previously worked with numerous non-profit mitochondrial patient organizations in which he served as co-chair and chair of the United Mitochondrial Disease Foundation (UMDF) grants committee, the UMDF Scientific and Medical Advisory Board, and the planning committee for the UMDF scientific symposiums.

The goal of his research group is to understand the role of the mitochondrial DNA replication machinery, namely POLG, in the production and prevention of mutations in mtDNA in health and disease and how the environment influences that process. His group was the first to discover and clone the human POLG and POLG2 genes followed by overexpression and characterization of the POLG and POLG2 proteins. He combines traditional biochemistry, enzymology, structural biology, yeast genetics and cell models to determine the consequences of POLG and similar disease mutations. His group maintains the human DNA polymerase gamma mutation database which has been useful to clinicians and families affected by POLG disorders.