Abstract
Erythrocyte formation involves the elimination of mitochondria at the reticulocyte stage of development. Nix-/- reticulocytes fail to eliminate their mitochondria at this step due to a defect in the targeting of mitochondria to autophagosomes. To determine the role of autophagy in this process, we generated Atg7-/- transplant mice. Atg7-/- reticulocytes exhibit a partial defect in mitochondrial clearance, demonstrating that there are both autophagy-dependent and -independent mechanisms of mitochondrial clearance. We used Atg7-/- autophagy-defective reticulocytes to study temporal events in mitochondrial clearance. Mitochondrial depolarization precedes elimination, but in Atg7-/- reticulocytes the depolarization event is markedly delayed. Since Atg7 regulates autophagosome formation, we infer that mitochondrial depolarization occurs downstream of autophagosome formation in reticulocytes. We propose that there are two mechanisms of mitochondrial clearance: one that is triggered by mitochondrial depolarization, and a second NIX-dependent mechanism, which is not. The NIX-dependent mechanism remains to be elucidated.
Original language | English (US) |
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Pages (from-to) | 1064-1065 |
Number of pages | 2 |
Journal | Autophagy |
Volume | 5 |
Issue number | 7 |
DOIs | |
State | Published - Oct 1 2009 |
Externally published | Yes |
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Keywords
- Atg7
- Autophagy
- Mitochondria
- Mitochondrial clearance
- Mitochondrial depolarization
- Mitophagy
- NIX
- Reticulocyte
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology
Cite this
Autophagy-dependent and -independent mechanisms of mitochondrial clearance during reticulocyte maturation. / Zhang, Ji; Ney, Paul A.
In: Autophagy, Vol. 5, No. 7, 01.10.2009, p. 1064-1065.Research output: Contribution to journal › Short survey
}
TY - JOUR
T1 - Autophagy-dependent and -independent mechanisms of mitochondrial clearance during reticulocyte maturation
AU - Zhang, Ji
AU - Ney, Paul A.
PY - 2009/10/1
Y1 - 2009/10/1
N2 - Erythrocyte formation involves the elimination of mitochondria at the reticulocyte stage of development. Nix-/- reticulocytes fail to eliminate their mitochondria at this step due to a defect in the targeting of mitochondria to autophagosomes. To determine the role of autophagy in this process, we generated Atg7-/- transplant mice. Atg7-/- reticulocytes exhibit a partial defect in mitochondrial clearance, demonstrating that there are both autophagy-dependent and -independent mechanisms of mitochondrial clearance. We used Atg7-/- autophagy-defective reticulocytes to study temporal events in mitochondrial clearance. Mitochondrial depolarization precedes elimination, but in Atg7-/- reticulocytes the depolarization event is markedly delayed. Since Atg7 regulates autophagosome formation, we infer that mitochondrial depolarization occurs downstream of autophagosome formation in reticulocytes. We propose that there are two mechanisms of mitochondrial clearance: one that is triggered by mitochondrial depolarization, and a second NIX-dependent mechanism, which is not. The NIX-dependent mechanism remains to be elucidated.
AB - Erythrocyte formation involves the elimination of mitochondria at the reticulocyte stage of development. Nix-/- reticulocytes fail to eliminate their mitochondria at this step due to a defect in the targeting of mitochondria to autophagosomes. To determine the role of autophagy in this process, we generated Atg7-/- transplant mice. Atg7-/- reticulocytes exhibit a partial defect in mitochondrial clearance, demonstrating that there are both autophagy-dependent and -independent mechanisms of mitochondrial clearance. We used Atg7-/- autophagy-defective reticulocytes to study temporal events in mitochondrial clearance. Mitochondrial depolarization precedes elimination, but in Atg7-/- reticulocytes the depolarization event is markedly delayed. Since Atg7 regulates autophagosome formation, we infer that mitochondrial depolarization occurs downstream of autophagosome formation in reticulocytes. We propose that there are two mechanisms of mitochondrial clearance: one that is triggered by mitochondrial depolarization, and a second NIX-dependent mechanism, which is not. The NIX-dependent mechanism remains to be elucidated.
KW - Atg7
KW - Autophagy
KW - Mitochondria
KW - Mitochondrial clearance
KW - Mitochondrial depolarization
KW - Mitophagy
KW - NIX
KW - Reticulocyte
UR - http://www.scopus.com/inward/record.url?scp=70349634803&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=70349634803&partnerID=8YFLogxK
U2 - 10.4161/auto.5.7.9749
DO - 10.4161/auto.5.7.9749
M3 - Short survey
C2 - 19713771
AN - SCOPUS:70349634803
VL - 5
SP - 1064
EP - 1065
JO - Autophagy
JF - Autophagy
SN - 1554-8627
IS - 7
ER -