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 mitochondrial dysfunction, primarily focusing on an intracellular signaling pathway known as the mitochondrial unfolded protein response (UPRmt). We have made significant progress toward understanding how cells monitor mitochondrial function and adapt transcription accordingly if the mitochondrial pool is compromised. Cells simply monitor mitochondrial protein import efficiency of the transcription factor ATFS-1. Normally, ATFS-1 is rapidly imported into mitochondria and degraded. However, mitochondrial dysfunction results in reduced import efficiency, allowing ATFS-1 to accumulate in the cytosol and subsequently traffic to the nucleus, where it adapts transcription. The transcriptional adaptations mediated by ATFS-1 suggest that cells stabilize the mitochondrial protein-folding environment, shift metabolism away from aerobic respiration, and coordinate both the mitochondrial and nuclear genomes to efficiently regenerate the respiratory chain to recover from mitochondrial dysfunction. 

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Selected Achievements

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)

At Work: Cell Biologist Cole Haynes

At Work: Cell Biologist Cole Haynes

Cell biologist Cole Haynes studies the stress responses that cells naturally mount to protect and maintain mitochondria.