NIX induces mitochondrial autophagy in reticulocytes

Ji Zhang, Paul A. Ney

Research output: Contribution to journalArticle

57 Scopus citations


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.1,2 NIX-deficient reticulocytes have a significant defect of mitochondrial clearance. Consistent with the ability of NIX to cause mitochondrial depolarization,3,4 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.

Original languageEnglish (US)
Pages (from-to)354-356
Number of pages3
Issue number3
StatePublished - Apr 1 2008
Externally publishedYes


  • Autophagy
  • BH3-only protein
  • Bcl-2 family
  • Beclin
  • Mitochondria
  • NIX
  • Organelle degradation
  • Reticulocyte

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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