Open Access
Proceedings of the National Academy of Sciences of the United States of America, volume 104, issue 28, pages 11649-11654
Bak regulates mitochondrial morphology and pathology during apoptosis by interacting with mitofusins
Brooks Craig
1
,
Wei Qingqing
1
,
Feng Leping
1
,
Dong Guie
1
,
Tao Yanmei
2
,
Lin Mei
2
,
Xie Zi-jian
3
,
Zheng Dong
1
1
*Department of Cellular Biology and Anatomy,
2
Institute of Molecular Medicine and Genomics, Medical College of Georgia and Veterans Affairs Medical Center, Augusta, GA 30912; and
|
3
Department of Physiology and Pharmacology, University of Toledo, Toledo, OH 43614
Publication type: Journal Article
Publication date: 2007-07-02
Quartile SCImago
Q1
Quartile WOS
Q1
Impact factor: 11.1
ISSN: 00278424, 10916490
PubMed ID:
17606912
Multidisciplinary
Abstract
Mitochondrial injury, characterized by outer membrane permeabilization and consequent release of apoptogenic factors, is a key to apoptosis of mammalian cells. Bax and Bak, two multidomain Bcl-2 family proteins, provide a requisite gateway to mitochondrial injury. However it is unclear how Bax and Bak cooperate to provoke mitochondrial injury and whether their roles are redundant. Here, we have identified a unique role of Bak in mitochondrial fragmentation, a seemingly morphological event that contributes to mitochondrial injury during apoptosis. We show that mitochondrial fragmentation is attenuated in Bak-deficient mouse embryonic fibroblasts, baby mouse kidney cells, and, importantly, also in primary neurons isolated from brain cortex of Bak-deficient mice. In sharp contrast, Bax deficiency does not prevent mitochondrial fragmentation during apoptosis. Bcl-2 and Bcl-XL inhibit mitochondrial fragmentation, and their inhibitory effects depend on the presence of Bak. Reconstitution of Bak into Bax/Bak double-knockout cells restores mitochondrial fragmentation, whereas reconstitution of Bax is much less effective. Bak interacts with Mfn1 and Mfn2, two mitochondrial fusion proteins. During apoptosis, Bak dissociates from Mfn2 and enhances the association with Mfn1. Mutation of Bak in the BH3 domain prevents its dissociation from Mfn2 and diminishes its mitochondrial fragmentation activity. This study has uncovered a previously unrecognized function of Bak in the regulation of mitochondrial morphological dynamics during apoptosis. By this function, Bak may collaborate with Bax to permeabilize the outer membrane of mitochondria, unleashing the apoptotic cascade.
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- We do not take into account publications that without a DOI.
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Brooks C. et al. Bak regulates mitochondrial morphology and pathology during apoptosis by interacting with mitofusins // Proceedings of the National Academy of Sciences of the United States of America. 2007. Vol. 104. No. 28. pp. 11649-11654.
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Brooks C., Wei Q., Feng L., Dong G., Tao Y., Lin M., Xie Z., Zheng D. Bak regulates mitochondrial morphology and pathology during apoptosis by interacting with mitofusins // Proceedings of the National Academy of Sciences of the United States of America. 2007. Vol. 104. No. 28. pp. 11649-11654.
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TY - JOUR
DO - 10.1073/pnas.0703976104
UR - https://doi.org/10.1073%2Fpnas.0703976104
TI - Bak regulates mitochondrial morphology and pathology during apoptosis by interacting with mitofusins
T2 - Proceedings of the National Academy of Sciences of the United States of America
AU - Brooks, Craig
AU - Wei, Qingqing
AU - Feng, Leping
AU - Dong, Guie
AU - Tao, Yanmei
AU - Lin, Mei
AU - Xie, Zi-jian
AU - Zheng, Dong
PY - 2007
DA - 2007/07/02 00:00:00
PB - Proceedings of the National Academy of Sciences (PNAS)
SP - 11649-11654
IS - 28
VL - 104
PMID - 17606912
SN - 0027-8424
SN - 1091-6490
ER -
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@article{2007_Brooks,
author = {Craig Brooks and Qingqing Wei and Leping Feng and Guie Dong and Yanmei Tao and Mei Lin and Zi-jian Xie and Dong Zheng},
title = {Bak regulates mitochondrial morphology and pathology during apoptosis by interacting with mitofusins},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
year = {2007},
volume = {104},
publisher = {Proceedings of the National Academy of Sciences (PNAS)},
month = {jul},
url = {https://doi.org/10.1073%2Fpnas.0703976104},
number = {28},
pages = {11649--11654},
doi = {10.1073/pnas.0703976104}
}
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Brooks, Craig, et al. “Bak regulates mitochondrial morphology and pathology during apoptosis by interacting with mitofusins.” Proceedings of the National Academy of Sciences of the United States of America, vol. 104, no. 28, Jul. 2007, pp. 11649-11654. https://doi.org/10.1073%2Fpnas.0703976104.