Heat Shock Proteins in the “Hot” Mitochondrion: Identity and Putative Roles

BioEssays - Tập 41 Số 9 - 2019
M. Nasr1,2, Г. И. Довбешко3, Stephen L. Bearne4,5, Nagwa El‐Badri1, Chérif F. Matta5,6,2,7
1Center of Excellence for Stem Cells and Regenerative Medicine (CESC), Zewail City of Science and Technology, 6th of October City, 12588, Egypt
2Department of Chemistry and Physics, Mount Saint Vincent University, Halifax, Nova Scotia B3M 2J6, Canada
3Department of Physics of Biological Systems Institute of Physics of the National Academy of Sciences of Ukraine Prospekt Nauki 46 Kiev 03039 Ukraine
4Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, Nova Scotia B3H 4R2, Canada
5Department of Chemistry, Dalhousie University, Halifax, Nova Scotia B3H 4R2, Canada
6Department of Chemistry, Saint Mary's University, Halifax, Nova Scotia, B3H 3C3 Canada
7Département de chimie Université Laval Québec Québec G1V 0A6 Canada

Tóm tắt

The mitochondrion is known as the “powerhouse” of eukaryotic cells since it is the main site of adenosine 5′‐triphosphate (ATP) production. Using a temperature‐sensitive fluorescent probe, it has recently been suggested that the stray free energy, not captured into ATP, is potentially sufficient to sustain mitochondrial temperatures higher than the cellular environment, possibly reaching up to 50 °C. By 50 °C, some DNA and mitochondrial proteins may reach their melting temperatures; how then do these biomolecules maintain their structure and function? Further, the production of reactive oxygen species (ROS) accelerates with temperature, implying higher oxidative stresses in the mitochondrion than generally appreciated. Herein, it is proposed that mitochondrial heat shock proteins (particularly Hsp70), in addition to their roles in protein transport and folding, protect mitochondrial proteins and DNA from thermal and ROS damage. Other thermoprotectant mechanisms are also discussed.

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