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Cole M. Haynes, PhD
Assistant Professor
Gerstner Sloan Kettering Graduate School of Biomedical Sciences
PhD, University of Missouri - Kansas City

Mailing Address:
New York , NY
Phone: 212-639-3451
Fax: 212-639-3452

Research Interests

Focus on the molecular mechanisms of mitochondrial function during development, aging, and cancer cell growth

Mitochondrial dysfunction is associated with multiple pathologies including Parkinson’s disease, cancer, bacterial infection, and metabolic disorders as well as general aging. The Haynes research group investigates how cells adapt to survive mitochondrial dysfunction, primarily focusing on an intracellular signaling pathway known as the mitochondrial unfolded protein response (UPRmt).

The Haynes lab has 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.

Currently, the lab utilizes C. elegans and mammalian systems to:

-Further understand how the UPRmt is regulated genetically and mechanistically.

-Determine how the UPRmt integrates with additional pathways activated during mitochondrial dysfunction, including mitophagy, to promote survival.

-Identify the metabolic pathways cells employ to survive mitochondrial dysfunction.

-Determine the role of the UPRmt during neurodegenerative conditions, cancers where mitochondrial dysfunction is prevalent, bacterial infection, and normal aging.




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