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Oxidative stress-induced autophagy in plants: The role of mitochondria

Authors
Journal
Plant Physiology and Biochemistry
0981-9428
Publisher
Elsevier
Volume
59
Identifiers
DOI: 10.1016/j.plaphy.2012.02.013
Keywords
  • Oxidized Proteins
  • Damaged Organelles
  • Autophagy
  • Autophagic Proteins
  • Mitochondria
  • Mitophagy
  • Cell Death
Disciplines
  • Biology

Abstract

Abstract The strictly regulated removal of oxidized structures is a universal stress response of eukaryotic cells that targets damaged or toxic components for vacuolar or lysosomal degradation. Autophagy stands at the crossroad between cell survival and death. It promotes survival by degrading proteins and organelles damaged during oxidative stress, but it is also activated as a part of death programs, when the damage cannot be overcome. Evidence is accumulating that the cellular sites of ROS production and signaling may be primary targets of autophagy. Therefore, autophagosomal targeting of mitochondria (mitophagy) is of particular importance. Mitophagy is a selective process that can specifically target dysfunctional mitochondria, but also mitophagy may play a role in controlling the number and quality of mitochondria during stress. Here we review the mechanisms of both non-specific autophagy and mitochondrial targeting in plants, drawing analogies and emphasizing differences with yeast and mammalian systems.

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