Abstract
Autophagy is a lysosome-dependent cellular degradation process. Organisms bearing deletions of the essential autophagy genes exhibit various pathological conditions, including cancer in mammals and shortened life span in C. elegans. The direct cause for these phenotypes is not clear. Here we used yeast as a model system to characterize the cellular consequence of ATG (autophagy-related) gene deletions. We found that the atg mutant strains, atg1Δ, atg6Δ, atg8Δ and atg12Δ, showed defects related to mitochondrial biology. These strains were unable to degrade mitochondria in stationary culture. In non-fermentable medium, which requires mitochondrial oxidative phosphorylation for survival, these atg strains showed a growth defect with an increased cell population at the G1 phase of the cell cycle. The cells had lower oxygen consumption rates and reduced mitochondrial electron transport chain activities. Under these growth conditions, the atg strains had lower mitochondrial membrane potential. In addition, these mutants generated higher levels of reactive oxygen species (ROS) and they were prone to accumulate dysfunctional mitochondria. This study clearly indicates that an autophagy defect has a functional impact on various aspects of mitochondrial functions and suggests a critical role of autophagy in mitochondria maintenance.
| Original language | English |
|---|---|
| Pages (from-to) | 337-346 |
| Number of pages | 10 |
| Journal | Autophagy |
| Volume | 3 |
| Issue number | 4 |
| Publication status | Published - Jul 2007 |
| Externally published | Yes |
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Keywords
- Autophagy
- Mitochondrial function
- Oxidative phosphorylation
- Petite
- Reactive oxygen species
- S. Cerevisiae
ASJC Scopus subject areas
- Cell Biology
- Molecular Biology
Cite this
The role of autophagy in mitochondria maintenance : Characterization of mitochondrial functions in autophagy-deficient S. cerevisiae strains. / Zhang, Yong; Qi, Haiyan; Taylor, Robert; Xu, Weihong; Liu, Leroy-Fong; Jin, Shengkan.
In: Autophagy, Vol. 3, No. 4, 07.2007, p. 337-346.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The role of autophagy in mitochondria maintenance
T2 - Characterization of mitochondrial functions in autophagy-deficient S. cerevisiae strains
AU - Zhang, Yong
AU - Qi, Haiyan
AU - Taylor, Robert
AU - Xu, Weihong
AU - Liu, Leroy-Fong
AU - Jin, Shengkan
PY - 2007/7
Y1 - 2007/7
N2 - Autophagy is a lysosome-dependent cellular degradation process. Organisms bearing deletions of the essential autophagy genes exhibit various pathological conditions, including cancer in mammals and shortened life span in C. elegans. The direct cause for these phenotypes is not clear. Here we used yeast as a model system to characterize the cellular consequence of ATG (autophagy-related) gene deletions. We found that the atg mutant strains, atg1Δ, atg6Δ, atg8Δ and atg12Δ, showed defects related to mitochondrial biology. These strains were unable to degrade mitochondria in stationary culture. In non-fermentable medium, which requires mitochondrial oxidative phosphorylation for survival, these atg strains showed a growth defect with an increased cell population at the G1 phase of the cell cycle. The cells had lower oxygen consumption rates and reduced mitochondrial electron transport chain activities. Under these growth conditions, the atg strains had lower mitochondrial membrane potential. In addition, these mutants generated higher levels of reactive oxygen species (ROS) and they were prone to accumulate dysfunctional mitochondria. This study clearly indicates that an autophagy defect has a functional impact on various aspects of mitochondrial functions and suggests a critical role of autophagy in mitochondria maintenance.
AB - Autophagy is a lysosome-dependent cellular degradation process. Organisms bearing deletions of the essential autophagy genes exhibit various pathological conditions, including cancer in mammals and shortened life span in C. elegans. The direct cause for these phenotypes is not clear. Here we used yeast as a model system to characterize the cellular consequence of ATG (autophagy-related) gene deletions. We found that the atg mutant strains, atg1Δ, atg6Δ, atg8Δ and atg12Δ, showed defects related to mitochondrial biology. These strains were unable to degrade mitochondria in stationary culture. In non-fermentable medium, which requires mitochondrial oxidative phosphorylation for survival, these atg strains showed a growth defect with an increased cell population at the G1 phase of the cell cycle. The cells had lower oxygen consumption rates and reduced mitochondrial electron transport chain activities. Under these growth conditions, the atg strains had lower mitochondrial membrane potential. In addition, these mutants generated higher levels of reactive oxygen species (ROS) and they were prone to accumulate dysfunctional mitochondria. This study clearly indicates that an autophagy defect has a functional impact on various aspects of mitochondrial functions and suggests a critical role of autophagy in mitochondria maintenance.
KW - Autophagy
KW - Mitochondrial function
KW - Oxidative phosphorylation
KW - Petite
KW - Reactive oxygen species
KW - S. Cerevisiae
UR - http://www.scopus.com/inward/record.url?scp=34250811414&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34250811414&partnerID=8YFLogxK
M3 - Article
C2 - 17404498
AN - SCOPUS:34250811414
VL - 3
SP - 337
EP - 346
JO - Autophagy
JF - Autophagy
SN - 1554-8627
IS - 4
ER -