Mitochondria removal by autophagy

Abstract

Mitochondrial dysfunction has severe cellular consequences and is linked with neurodegenerative diseases and aging. Maintaining a healthy population of mitochondria is thus essential for proper cellular homeostasis. Several strategies have evolved to prevent and limit mitochondria damage, and macroautophagy plays a role in degrading superfluous or severely damaged mitochondria. Selective removal of mitochondria by autophagy (termed mitophagy) has been extensively studied recently in both yeast and mammalian cells. In this review, we summarize our current knowledge of mitophagy. We also compare the molecular process of mitophagy with other types of specific autophagic pathways and discuss its biological importance.

Figure 1

Selective autophagy and the corresponding organelle marker, receptor and adaptor proteins. The Atg11 interaction domain of Atg32 has not been mapped at present and the indicated position is approximate. (A) Key motifs of the marker and receptor proteins; (B) Atg8/LC3 interaction motifs of autophagic marker and receptor proteins; (C) Models of selective autophagy in different organisms. Atg32 shares properties of both organelle/cargo marker proteins and receptors; it is an integral membrane component of the mitochondria, and it binds both Atg11 and Atg8. TMD, transmembrane domain; UBA, ubiquitin-associated domain.