scholarly journals Mitochondrial Fusion in Yeast Requires the Transmembrane GTPase Fzo1p

1998 ◽  
Vol 143 (2) ◽  
pp. 359-373 ◽  
Author(s):  
Greg J. Hermann ◽  
John W. Thatcher ◽  
John P. Mills ◽  
Karen G. Hales ◽  
Margaret T. Fuller ◽  
...  
Keyword(s):  
Mitochondrial Membrane ◽  
Fusion Reaction ◽  
Point Mutations ◽  
Integral Membrane Protein ◽  
Mitochondrial Fusion ◽  
Inner Mitochondrial Membrane ◽  
Fusion Event ◽  
Gtpase Domain ◽  
Developmentally Regulated ◽  
Mitochondrial Reticulum

Membrane fusion is required to establish the morphology and cellular distribution of the mitochondrial compartment. In Drosophila, mutations in the fuzzy onions (fzo) GTPase block a developmentally regulated mitochondrial fusion event during spermatogenesis. Here we report that the yeast orthologue of fuzzy onions, Fzo1p, plays a direct and conserved role in mitochondrial fusion. A conditional fzo1 mutation causes the mitochondrial reticulum to fragment and blocks mitochondrial fusion during yeast mating. Fzo1p is a mitochondrial integral membrane protein with its GTPase domain exposed to the cytoplasm. Point mutations that alter conserved residues in the GTPase domain do not affect Fzo1p localization but disrupt mitochondrial fusion. Suborganellar fractionation suggests that Fzo1p spans the outer and is tightly associated with the inner mitochondrial membrane. This topology may be required to coordinate the behavior of the two mitochondrial membranes during the fusion reaction. We propose that the fuzzy onions family of transmembrane GTPases act as molecular switches to regulate a key step in mitochondrial membrane docking and/or fusion.

scholarly journals ROMO1 is essential for glucose coupling in the pancreatic β cell of male mice

2021 ◽  
Author(s):  
Lisa Wells ◽  
Caterina Iorio ◽  
Andy Cheuk-Him Ng ◽  
Courtney Reeks ◽  
Siu-Pok Yee ◽  
...  
Keyword(s):  
Mitochondrial Membrane ◽  
Mitochondrial Dynamics ◽  
Critical Role ◽  
Physiological Role ◽  
Glucose Sensing ◽  
Mitochondrial Fusion ◽  
Male Mice ◽  
Inner Mitochondrial Membrane ◽  
Β Cell ◽  
Respiratory Capacity

AbstractReactive oxygen species modulator 1 (ROMO1) is a highly conserved inner mitochondrial membrane protein that senses ROS and regulates mitochondrial dynamics 1. ROMO1 is required for mitochondrial fusion in vitro, and silencing ROMO1 increases sensitivity to cell death stimuli. How ROMO1 promotes mitochondrial fusion and its physiological role remain unclear. Here we show that ROMO1 is essential for embryonic development, as ROMO1-null mice die before embryonic day 8.5, earlier than GTPases OPA1 or MFN1/2 that catalyze mitochondrial membrane fusion. Knockout of ROMO1 in adult pancreatic β cells results in impaired glucose homeostasis in male mice due to an insulin secretion defect resulting from impaired glucose sensing. Mitochondria in ROMO1 β cell KO cells were swollen and fragmented, consistent with a role for ROMO1 in mitochondrial fusion in vivo. While basal respiration was normal in ROMO1β cell KO islets, spare respiratory capacity was lost. Taken together, our data indicate that ROMO1 is required for nutrient coupling in the β cell and point to a critical role for spare respiratory capacity in the maintenance of euglycemia in males.

scholarly journals The BCL-2–like protein CED-9 of C. elegans promotes FZO-1/Mfn1,2– and EAT-3/Opa1–dependent mitochondrial fusion

2009 ◽  
Vol 186 (4) ◽  
pp. 525-540 ◽  
Author(s):  
Stéphane G. Rolland ◽  
Yun Lu ◽  
Charles N. David ◽  
Barbara Conradt
Keyword(s):  
Caenorhabditis Elegans ◽  
Mitochondrial Membrane ◽  
Muscle Cells ◽  
Mitochondrial Fusion ◽  
Mitochondrial Morphology ◽  
Inner Mitochondrial Membrane ◽  
C Elegans

The mammalian dynamin-related guanosine triphosphatases Mfn1,2 and Opa1 are required for mitochondrial fusion. However, how their activities are controlled and coordinated is largely unknown. We present data that implicate the BCL-2–like protein CED-9 in the control of mitochondrial fusion in Caenorhabditis elegans. We demonstrate that CED-9 can promote complete mitochondrial fusion of both the outer and inner mitochondrial membrane. We also show that this fusion is dependent on the C. elegans Mfn1,2 homologue FZO-1 and the C. elegans Opa1 homologue EAT-3. Furthermore, we show that CED-9 physically interacts with FZO-1 in vivo and that the ability of CED-9 to interact with FZO-1 is important for its ability to cause mitochondrial fusion. CED-9–induced mitochondrial fusion is not required for the maintenance of mitochondrial morphology during embryogenesis or in muscle cells, at least under normal conditions and in the absence of stress. Therefore, we propose that the BCL-2–like CED-9 acts through FZO-1/Mfn1,2 and EAT-3/Opa1 to promote mitochondrial fusion in response to specific cellular signals.

Translocase of inner mitochondrial membrane 44 alters the mitochondrial fusion and fission dynamics and protects from type 2 diabetes

Metabolism ◽  
2015 ◽  
Vol 64 (6) ◽  
pp. 677-688 ◽  
Author(s):  
Yu Wang ◽  
Akihiro Katayama ◽  
Takahiro Terami ◽  
Xiaoying Han ◽  
Tomokazu Nunoue ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Mitochondrial Membrane ◽  
Mitochondrial Fusion ◽  
Inner Mitochondrial Membrane

Modulation of the calcium-activated BK-channel of the inner mitochondrial membrane by hypoxia

2007 ◽  
Vol 34 (S 2) ◽  
Author(s):  
D Siemen ◽  
Y Cheng ◽  
X Gu ◽  
P Bednarczyk ◽  
GG Haddad ◽  
...  
Keyword(s):  
Mitochondrial Membrane ◽  
Bk Channel ◽  
Inner Mitochondrial Membrane

The Efects of Spaceflight on Mitochondria in Human Lymphocytes (Jurkat).

1999 ◽  
Vol 5 (S2) ◽  
pp. 1118-1119
Author(s):  
Heide Schatten ◽  
Marian Lewis
Keyword(s):  
Mitochondrial Membrane ◽  
Space Shuttle ◽  
Human Lymphocytes ◽  
Jurkat Cells ◽  
Apoptotic Bodies ◽  
Inner Mitochondrial Membrane ◽  
Mitochondrial Alterations ◽  
Mitochondrial Volume ◽  
Number Of Cells ◽  
Related Increase

Spaceflight induced mitochondrial alterations have been reported for muscle and may be associated with altered physiological functions in space. Mitochondrial alterations are also indicative of preapoptotic events which are seen in greater amounts in cells exposed to spaceflight when compared with cells cultured at 1 g. Preapoptotic mitochondrial changes include alterations of processes at the inner mitochondrial membrane and can result in changes in mitochondrial volume. Higher amounts of oxidative stress during space flight may be one of the causes for changes which lead to apoptosis. Jurkat cells flown on the STS-76 space shuttle mission showed an increase in the number of cells with apoptotic bodies early in the mission and a time-dependent, microgravity-related increase in the Fas/APO-1 cell death factor. Here we investigated the morphology of mitochondria in Jurkat cells exposed to spaceflight during the STS-76 mission.

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