American biologist
Marcia Carmen Haigis is an American biologist and professor in the Department of Cell Biology at Harvard Medical School. Her research looks to understand the metabolic circuitry of mitochondria, and how it impacts human health and disease. She was elected to the National Academy of Medicine in 2024.
Early life and education
Haigis was born in Las Vegas and moved to South Korea as a child. Her father was an officer in the United States Air Force. Haigis spent her early life moving between Nebraska and Alabama, before settling in Portsmouth, New Hampshire.[1] She was a freshman at the University of New Hampshire.[1] Here she trained as an emergency medical technician, accumulating hours of experience to be a member of the ambulance corps.[1] During her undergraduate studies Haigis discovered medical research, and spent her summers as a lab intern working on protein chemistry. Haigis trained in biochemistry at the University of Wisconsin–Madison. Her doctoral research looked to understand the mechanisms of toxic ribonuclease.[2] She learned a lot about protein folding and Sirtuin 1.[1] She was a postdoctoral researcher at the Massachusetts Institute of Technology, where she specialized in mitochondrial metabolics with Leonard P. Guarente.[1] Here she started working on SIRT3, SIRT4 and SIRT5. Amongst her many findings, she showed that SIRT4 repressed glutamate dehydrogenase 1, which suppressed insulin secretion.[1]
Research and career
Haigis looks to understand the role of mitochondria in human health.[3] In particular, Haigis has studied how the enzymatic networks in the mitochondrion modulate a cell's metabolism.[1] She joined the Harvard Medical School in 2006. One of her first graduate students, Lydia W. S. Finley, demonstrated that expression of genes critical to glycolysis was boosted when SIRT3 decreased.[1] The SIRT3 gene is the most depleted in tumor cells – it drives cancel cell proliferation, and mice lacking in SIRT3 result in mice spontaneously developing breast tumors.
Haigis has demonstrated the role of mitochondrial sirtuins (a protein family involved in the regulation of biological processes) in metabolism and disease. She revealed that ammonia, a metabolic waste product that is lethal to most biological tissue, was used to boost the growth of cancer cells.[1] She has shown that damage to DNA (which can accelerate cancer) activates the SIRT4 gene, and mice lacking SIRT4 developed spontaneous lung tumors.[1] Her lab also demonstrated that prolyl-hydroxylase 3 (PHD3), a signaling enzyme, breaks down fats inside the mitochondrion, and is suppressed in a subset of cancers (including acute myeloid leukemia).[1]
Awards and honors
Select publications
References
