共 48 条
Sar1, a Novel Regulator of ER-Mitochondrial Contact Sites
被引:19
作者:
Ackema, Karin B.
[1
]
Prescianotto-Baschong, Cristina
[1
]
Hench, Jurgen
[2
]
Wang, Shyi Chyi
[3
]
Chia, Zhi Hui
[3
]
Mergentaler, Heidi
[1
]
Bard, Frederic
[3
]
Frank, Stephan
[2
]
Spang, Anne
[1
]
机构:
[1] Univ Basel, Growth & Dev, Biozentrum, CH-4056 Basel, Switzerland
[2] Univ Basel Hosp, Inst Pathol, Div Neuropathol, CH-4031 Basel, Switzerland
[3] Inst Mol & Cell Biol, Singapore 138673, Singapore
来源:
基金:
瑞士国家科学基金会;
关键词:
EARLY SECRETORY PATHWAY;
OUTER-MEMBRANE PROTEIN;
SACCHAROMYCES-CEREVISIAE;
ENDOPLASMIC-RETICULUM;
C-ELEGANS;
CAENORHABDITIS-ELEGANS;
COPII VESICLE;
YEAST;
COMPLEX;
GTPASE;
D O I:
10.1371/journal.pone.0154280
中图分类号:
O [数理科学和化学];
P [天文学、地球科学];
Q [生物科学];
N [自然科学总论];
学科分类号:
07 ;
0710 ;
09 ;
摘要:
Endoplasmic reticulum (ER)-mitochondrial contact sites play a pivotal role in exchange of lipids and ions between the two organelles. How size and function of these contact sites are regulated remains elusive. Here we report a previously unanticipated, but conserved role of the small GTPase Sar1 in the regulation of ER-mitochondrial contact site size. Activated Sar1 introduces membrane curvature through its N-terminal amphiphatic helix at the ER-mitochondria interphase and thereby reducing contact size. Conversely, the S. cerevisiae N3-Sar1 mutant, in which curvature induction is decreased, caused an increase in ER-mitochondrial contacts. As a consequence, ER tubules are no longer able to mark the prospective scission site on mitochondria, thereby impairing mitochondrial dynamics. Consistently, blocking mitochondrial fusion partially rescued, whereas deletion of the dynamin-like protein enhanced the phenotype in the sar1D32G mutant. We conclude that Sar1 regulates the size of ER-mitochondria contact sites through its effects on membrane curvature.
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页数:16
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