4.8 Editorial Material

An unconventional pathway for mitochondrial protein degradation

Journal

AUTOPHAGY
Volume 12, Issue 11, Pages 1971-1972

Publisher

TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2016.1235127

Keywords

autophagy; mitochondrial-derived compartment; mitophagy; stress; yeast

Categories

Funding

  1. NIGMS NIH HHS [R01 GM053396] Funding Source: Medline
  2. NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM053396] Funding Source: NIH RePORTER

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Many vital metabolic pathways take place in mitochondria, but some of the associated processes generate toxic substances including reactive oxygen species that can damage proteins and DNA. Therefore, it is critical to maintain normally functioning mitochondria to achieve proper cellular homeostasis. Along these lines, mitochondrial dysfunction is associated with numerous diseases, and mitochondria quality control is essential for cell survival. The maintenance of functioning mitochondria is particularly important in aging cells, and there is a strong relationship between cellular aging and dysfunctional mitochondria. The best characterized pathway that is responsible for the elimination of damaged mitochondria is mitophagy, a selective type of autophagy. In yeast, mitophagy requires the mitochondrial protein Atg32 to serve as a receptor for recognition and sequestration by a phagophore. Although conventional mitophagy has been extensively studied, recent research suggests that an unconventional pathway, which is independent of Atg32, contributes to the removal of mitochondria.

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