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Rebooting Mitochondria With Adenosine Monophosphate

Cell Metabolism: The cell’s powerhouse recycles when AMP signals an alarm

by Sarah Everts
January 18, 2016 | APPEARED IN VOLUME 94, ISSUE 3

Credit: Salk Institute for Biological Studies
When mitochondria (left) are exposed to the toxin rotenone and start to degrade, AMP signals the organelle to save useful components in vesicles and reboot (right).

When cell mitochondria are exposed to electron-transport-chain poisons such as rotenone, the chemical-energy-producing organelles reboot themselves. First, mitochondria reorganize their valuable biomolecular contents into smaller vesicles. This segregation allows mitochondria to initiate degradation and recycling of damaged machinery. If the repair is not sufficient, then the entire cell dies. But often mitochondria are rebuilt using both new and recycled molecules in a process called fragmentation. Researchers led by Reuben J. Shaw at the Salk Institute for Biological Studies have found that adenosine monophosphate (AMP) is a master switch for fragmentation (Science 2016, DOI: 10.1126/science.aab4138). AMP is produced when the mitochondria’s chemical energy currency, adenosine triphosphate, loses two energy-rich phosphate groups. Its presence is a signal that mitochondria may not be functioning efficiently. Shaw and his team discovered AMP’s rebooting role when they found that a protein kinase activated by AMP is sufficient to kick-start the fragmentation process. A better understanding of mitochondrial recycling may provide insight to scientists developing drugs for diseases that affect mitochondria, such as Parkinson’s disease.



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