The Haynes Laboratory is interested in how cells and organisms adapt to mitochondrial dysfunction in a number of physiologic and pathologic scenarios including during aging, oocyte biogenesis, cancer cell growth, stem cell maintenance and bacterial infection. Mitochondrial dysfunction is a common factor to many human diseases, however the intrinsic means cells employ to survive and ultimately recover from mitochondrial perturbations are only beginning to be understood. We primarily focus on a intracellular signaling pathway known as the mitochondrial unfolded protein response (or UPR^mt), which allows cells to monitor the function of the entire cellular pool of mitochondria and adapt transcription accordingly. Using both C. elegans and mammalian models, we have significant progress in understanding the signal transduction mechanism as well its biological roles. Going forward, we hope to gain further insight into the mitochondrial contribution to human pathology and aging, and ultimately, manipulate the UPR^mt therapeutically.

Featured Publications

Lin YF, Schulz AM, Pellegrino MW, Lu Y, Shaham S, Haynes CM. (2016) Maintenance and propagation of a deleterious mitochondrial genome by the mitochondrial unfolded protein response. Nature. May 2:533(7603): 416-419.