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A key molecular step required for the division of damaged mitochondria—essential for cell health—has been identified by a University of Bristol-led study. The finding has the potential to establish how mitochondrial dysfunction goes wrong in common neurodegenerative diseases, such as Parkinson's and Alzheimer's.

The research is published in the journal Science Advances.

The main function of mitochondria is to generate the energy necessary to power cells. Present in nearly all types of human cell, mitochondria are vital to human survival. Mitochondria are also involved in other tasks, such as signaling, regulation of cellular metabolism, and cell death.

Mitochondrial fission factor (MFF) works by recruiting a secondary protein (DRP1) to the mitochondria to encourage division. However, the molecular details of how this happens are not fully understood.

The research team has identified a key protein in mitochondrial division, mitochondrial fission factor (MFF), as a target of a specific type of modification the lab specializes in called small ubiquitin-like modifier (SUMO).

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