Mitochondrial dysfunction is associated with multiple pathologies including Parkinson’s disease, cancer, bacterial infection, and metabolic disorders as well as general aging. We investigate how cells adapt to survive the cause of mitochondrial dysfunction and ultimately recover mitochondrial activity.
We primarily focus on an intracellular signaling pathway known as the mitochondrial unfolded protein response (UPRmt).We’ve made significant progress towards understanding how cells monitor mitochondrial function and adapt transcription accordingly if the mitochondrial pool is compromised. Cells simply monitor mitochondrial protein import efficiency using the transcription factor ATFS-1 as a sentinel.
Cole Haynes, PhD
Research FocusCell biologist Cole Haynes focuses on the molecular mechanisms of mitochondrial function during development, aging, and cancer cell growth.
- PhD, University of Missouri Kansas City
- Nargund AN, Fiorese CJ, Pellegrino MW, Deng P, Haynes CM. (2015) Mitochondrial and nuclear accumulation of the transcription factor ATFS-1 promotes OXPHOS recovery during the UPRmt. Mol Cell. April 2;58(1): 123-33.
- Pellegrino MW, Nargund AM, Kirienko NV, Gillis R, Fiorese CJ, Haynes CM. Mitochondrial UPR-regulated innate immunity provides resistance to pathogen infection. Nature. 2014. Sept 28. doi: 10.1038/nature13818
- Bristol-Myers Squibb/James D. Robinson III Junior Faculty Chair (2014)
- Boyer Award in Basic Research (2014)
- Ellison Medical Foundation New Scholar in Aging (2011)
- Gerstner Young Investigator (2010)
- Alfred W. Bressler Scholar (2010)