NIX induces mitochondrial autophagy in reticulocytes

Ji Zhang, Paul A. Ney

Research output: Contribution to journalArticle

51 Citations (Scopus)

Abstract

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
JournalAutophagy
Volume4
Issue number3
DOIs
StatePublished - Apr 1 2008
Externally publishedYes

Fingerprint

Reticulocytes
Autophagy
Erythroid Cells
Mitochondria
Cardiac Myocytes
Lenses
Homeostasis
Erythrocytes
Epithelial Cells
Maintenance
Neurons
Health
Proteins

Keywords

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

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

Cite this

NIX induces mitochondrial autophagy in reticulocytes. / Zhang, Ji; Ney, Paul A.

In: Autophagy, Vol. 4, No. 3, 01.04.2008, p. 354-356.

Research output: Contribution to journalArticle

Zhang, Ji ; Ney, Paul A. / NIX induces mitochondrial autophagy in reticulocytes. In: Autophagy. 2008 ; Vol. 4, No. 3. pp. 354-356.
@article{b8c13ded253c4956bc78b9c703d45e90,
title = "NIX induces mitochondrial autophagy in reticulocytes",
abstract = "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.",
keywords = "Autophagy, Bcl-2 family, Beclin, BH3-only protein, Mitochondria, NIX, Organelle degradation, Reticulocyte",
author = "Ji Zhang and Ney, {Paul A.}",
year = "2008",
month = "4",
day = "1",
doi = "10.4161/auto.5552",
language = "English (US)",
volume = "4",
pages = "354--356",
journal = "Autophagy",
issn = "1554-8627",
publisher = "Landes Bioscience",
number = "3",

}

TY - JOUR

T1 - NIX induces mitochondrial autophagy in reticulocytes

AU - Zhang, Ji

AU - Ney, Paul A.

PY - 2008/4/1

Y1 - 2008/4/1

N2 - 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.

AB - 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.

KW - Autophagy

KW - Bcl-2 family

KW - Beclin

KW - BH3-only protein

KW - Mitochondria

KW - NIX

KW - Organelle degradation

KW - Reticulocyte

UR - http://www.scopus.com/inward/record.url?scp=41449115693&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=41449115693&partnerID=8YFLogxK

U2 - 10.4161/auto.5552

DO - 10.4161/auto.5552

M3 - Article

VL - 4

SP - 354

EP - 356

JO - Autophagy

JF - Autophagy

SN - 1554-8627

IS - 3

ER -