Marcia C. Haigis
Who she is
Marcia C. Haigis obtained her Ph.D. in Biochemistry from the University of Wisconsin in 2002. She then performed postdoctoral research at MIT studying the biology of aging and mitochondrial metabolism. In 2006, Dr. Haigis joined the faculty of Harvard Medical School, where she is currently an Associate Professor in the Department of Cell Biology. Additionally, Dr. Haigis is an active member of the Paul F. Glenn Laboratories for Medical Research.
What she does
An overarching goal of the Haigis lab is to understand the role that mitochondria play in human health, aging and age-related diseases. In particular, the lab is working to identify new molecular mechanisms that allow mitochondria to mediate cellular adaptation to stress.
These studies have led to a deeper understanding of how mitochondria reprogram metabolism in response to cellular stress and identification of novel molecular mechanisms involved in this reprogramming. In their work, Haigis lab researchers have discovered new physiological processes regulated by mitochondrial sirtuins, which function as NAD-dependent deacetylases, deacylases or ADP-ribosyltransferases.
For example, using a platform of metabolomics, signaling, mitochondrial biochemistry and cell biology, the group has discovered that the mitochondrial deacetylase SIRT3 represses the Warburg effect in tumor cells, controlling cancer cell metabolism via a mitochondrial signaling pathway. These studies have the potential to lead to novel therapies that could treat a spectrum of human diseases.
News from the Lab
Recent studies in the Haigis laboratory have focused on elucidating metabolic reprogramming that allows cells to adapt to stress. The team has discovered a novel, ‘metabolic checkpoint’ that is induced in cells upon exposure to DNA damage. Many tumor cells undergo metabolic reprograming of glutamine metabolism, which provides precursors to support increased biosynthesis and redox control. Haigis lab’s work showed that cells lacking this metabolic checkpoint in response to stress experience high levels of genomic instability and transformation. The lab’s researchers are continuing this work to identify new molecular regulators that link mitochondria with metabolic checkpoints.