Document Detail

NIX induces mitochondrial autophagy in reticulocytes.
MedLine Citation:
PMID:  18623629     Owner:  NLM     Status:  MEDLINE    
The controlled elimination of defective mitochondria is necessary for the health of long-lived post-mitotic cells, like cardiomyocytes and neurons. Mitochondrial elimination also occurs during the course of normal development, in lens epithelial and erythroid cells. Strikingly, at the final stage of erythroid cell maturation, newly formed erythrocytes, also known as reticulocytes, eliminate their entire cohort of mitochondria. We have employed this model to investigate the mechanism of programmed mitochondrial clearance. NIX (BNIP3L) is a Bcl-2-related protein that is upregulated during terminal erythroid differentiation. NIX-deficient reticulocytes have a significant defect of mitochondrial clearance. Consistent with the ability of NIX to cause mitochondrial depolarization, we show that mitochondria are depolarized in wild type but not NIX deficient reticulocytes. NIX does not function through established proapoptotic pathways, nor does it mediate the induction of autophagy in erythroid cells. Rather, NIX is required for the selective incorporation of mitochondria into autophagosomes. Elucidation of the mechanism of this effect will improve our understanding of the role of autophagy in the maintenance of cellular homeostasis.
Ji Zhang; Paul A Ney
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Autophagy     Volume:  4     ISSN:  1554-8635     ISO Abbreviation:  Autophagy     Publication Date:  2008 Apr 
Date Detail:
Created Date:  2008-07-11     Completed Date:  2008-07-23     Revised Date:  2014-09-21    
Medline Journal Info:
Nlm Unique ID:  101265188     Medline TA:  Autophagy     Country:  United States    
Other Details:
Languages:  eng     Pagination:  354-6     Citation Subset:  IM    
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MeSH Terms
Autophagy / physiology*
Cell Differentiation
Membrane Proteins / genetics,  physiology*
Mice, Knockout
Mitochondria / physiology*
Mitochondrial Proteins / genetics,  physiology*
Phagosomes / physiology
Reticulocytes / physiology*,  ultrastructure
bcl-2 Homologous Antagonist-Killer Protein / physiology
bcl-2-Associated X Protein / physiology
Grant Support
R21 DK074519/DK/NIDDK NIH HHS; R21 DK074519-01/DK/NIDDK NIH HHS; R21 DK074519-02/DK/NIDDK NIH HHS
Reg. No./Substance:
0/Bak1 protein, mouse; 0/Bax protein, mouse; 0/Membrane Proteins; 0/Mitochondrial Proteins; 0/Nix protein, mouse; 0/bcl-2 Homologous Antagonist-Killer Protein; 0/bcl-2-Associated X Protein

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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