Selective mitochondrial autophagy during erythroid maturation.
Accumulating evidence suggests that autophagy can be selective in the clearance of organelles in yeast and in mammalian cells. We have observed that the sequestration of mitochondria by autophagosomes was defective in reticulocytes in the absence of Nix. Nix is required for the dissipation of mitochondrial membrane potential (DeltaPsim) during erythroid maturation. Moreover, pharmacological agents that induce the loss of DeltaPsim can restore the sequestration of mitochondria by autophagosomes and promote mitochondrial clearance in Nix(-/-) erythroid cells. Our data suggest that mitochondrial depolarization induces recognition and sequestration of mitochondria by autophagosomes. Elucidating the mechanisms underlying selective mitochondrial autophagy not only will help us to understand the mechanisms for erythroid maturation, but also may provide insights into mitochondrial quality control by autophagy in the protection against aging, cancer and neurodegenerative diseases.
Chen
Min
M
Department of Immunology, Baylor College of Medicine, Houston, Texas 77030, USA. minc@bcm.tmc.edu
Sandoval
Hector
H
Wang
Jin
J
D000743:Anemia, Hemolytic / Q000235:genetics / Q000473:pathology; D000818:Animals; D001343:Autophagy; D004920:Erythropoiesis / Q000235:genetics / Q000502:physiology*; D006801:Humans; D053078:Membrane Potential, Mitochondrial; D008565:Membrane Proteins / Q000235:genetics / Q000502:physiology*; D051379:Mice; D008928:Mitochondria / Q000502:physiology*; D024101:Mitochondrial Proteins / Q000235:genetics / Q000502:physiology*; D012156:Reticulocytes / Q000502:physiology* / Q000648:ultrastructure
D008565:Membrane Proteins; D024101:Mitochondrial Proteins; C501741:Nix protein, mouse