ライフサイエンスコーパス: mitochondrial fusion

1 duced oxidative phosphorylation and enhanced mitochondrial fusion.

2 ) as new Smad2 binding partners required for mitochondrial fusion.

3 mportant and elusive process of MFN-mediated mitochondrial fusion.

4 bc13 inactivation abrogates parkin-dependent mitochondrial fusion.

5 ion, suppressing mitophagy without impairing mitochondrial fusion.

6 al respiratory capacity, ATP production, and mitochondrial fusion.

7 otypes are not necessarily caused by altered mitochondrial fusion.

8 association, which is a necessary prelude to mitochondrial fusion.

9 to s-OPA1, indicating that s-OPA1 regulates mitochondrial fusion.

10 on is necessary for increased IHG-1-mediated mitochondrial fusion.

11 , a molecule required for maintaining proper mitochondrial fusion.

12 h long and short forms of OPA1 and maintains mitochondrial fusion.

13 of YAP2 in human cell lines causes increased mitochondrial fusion.

14 morphology and have overlapping functions in mitochondrial fusion.

15 gulates the lipid and protein machineries of mitochondrial fusion.

16 where SMS deficient MSCs show high levels of mitochondrial fusion.

17 phosphorylation sites, leading to unopposed mitochondrial fusion.

18 Further, MODE 2 sequestration prevents mitochondrial fusion.

19 ondrial transport, distinct from its role in mitochondrial fusion.

20 een Fzo1 GTP hydrolysis, ubiquitylation, and mitochondrial fusion.

21 FZO-1 is important for its ability to cause mitochondrial fusion.

22 hosphatases Mfn1,2 and Opa1 are required for mitochondrial fusion.

23 optic atrophy 1 (OPA1), the key proteins for mitochondrial fusion.

24 ity in cells that regulates apoptosis and/or mitochondrial fusion.

25 In yeast, three proteins are essential for mitochondrial fusion.

26 on requires increased OXPHOS as supported by mitochondrial fusion.

27 ropathy, result from a primary deficiency of mitochondrial fusion.

28 eukaryote cells, playing a critical role in mitochondrial fusion.

29 oss of GSCs that was caused by inhibition of mitochondrial fusion.

30 uces mitochondrial fragmentation by blocking mitochondrial fusion.

31 of RAGA-1 increases lifespan via maintaining mitochondrial fusion.

32 fusins 1 and 2, the predominant catalysts of mitochondrial fusion.

33 s, Mfn1 and Mfn2, are required for efficient mitochondrial fusion.

34 ell physiologies that require high levels of mitochondrial fusion.

35 Both increases are supported by mitochondrial fusion.

36 L2 and upstream of the mitofusins to promote mitochondrial fusion.

37 ic animals is also associated with depressed mitochondrial fusion.

38 namin-related GTPases that are essential for mitochondrial fusion.

39 quitin ligases Mdm30 and Rsp5 that modulates mitochondrial fusion.

40 d interaction of MYO2 and genes required for mitochondrial fusion.

41 levels of Fzo1 and maintenance of efficient mitochondrial fusion.

42 nduction of mitochondrial beta-oxidation and mitochondrial fusion.

43 ochondrial outer membrane protein regulating mitochondrial fusion, a dynamic process essential for mi

44 on of tubulin and that loss of CCP1-mediated mitochondrial fusion accounts for the exquisite vulnerab

45 Our results suggest that disruption of mitochondrial fusion activates multiple stress response

46 and excessive mitochondrial fission, enhance mitochondrial fusion activity and protect cells.

47 Drp1 activity and shifts the balance toward mitochondrial fusion, adding another layer of complexity

48 ystems has shown that Mfn-2 is a mediator of mitochondrial fusion, an evolutionarily conserved proces

49 cts of LYCAT were mediated by an increase in mitochondrial fusion and a G(1)/S cell cycle transition,

50 , overexpression of IHG-1 leads to increased mitochondrial fusion and also protects cells from reacti

51 Bcl2l13 expression correlated with increased mitochondrial fusion and biogenesis.

52 N2 (the gene encoding mitofusin 2) interrupt mitochondrial fusion and cause the untreatable neurodege

53 SPRY2 KD cells displayed impaired mitochondrial fusion and cell membrane damage, explainin

54 Pase that plays a central role in regulating mitochondrial fusion and cell metabolism.

55 PGAM5 deletion leads to increased mitochondrial fusion and decreased mitochondrial turnove

56 el analysis, we further dissect the steps of mitochondrial fusion and demonstrate that the mutant var

57 els and that HTT mediates FMRP regulation of mitochondrial fusion and dendritic maturation.

58 oteins Fzo1 and Dnm1, which are required for mitochondrial fusion and division, respectively.

59 Ablation of the mitochondrial fusion and endoplasmic reticulum (ER)-teth

60 Here, we examined mitochondrial fusion and energetic activities in cells p

61 t the differential roles of L- and S-OPA1 in mitochondrial fusion and energetics are ill-defined.

62 Mitochondrial fusion and fission affect the distribution

63 Mitochondrial fusion and fission appear essential for he

64 Because of these important functions, mitochondrial fusion and fission are essential in mammal

65 Mitochondrial fusion and fission are mediated by several

66 ific mitochondrial autophagy (mitophagy) and mitochondrial fusion and fission are protective quality

67 on the intimate relationship between normal mitochondrial fusion and fission balances, as influenced

68 The forms of the cristae during mitochondrial fusion and fission can be clearly observed

69 the first time that retuning the balance of mitochondrial fusion and fission can restore tissue inte

70 Surprisingly, cells deficient in mitochondrial fusion and fission distributed and inherit

71 PLD6 alters mitochondrial fusion and fission dynamics downstream of

72 Disturbed mitochondrial fusion and fission have been linked to var

73 In this article, we investigate beta-cell mitochondrial fusion and fission in detail and report al

74 ROS also shift the balance between mitochondrial fusion and fission in favor of increased f

75 eplication, thus revealing crucial roles for mitochondrial fusion and fission in maintaining the inte

76 Some of the major molecules mediating mitochondrial fusion and fission in mammals have been di

77 ing the mechanisms underlying the control of mitochondrial fusion and fission is critical to understa

78 is a novel regulatory factor controlling the mitochondrial fusion and fission machinery.

79 These data suggest that alterations in mitochondrial fusion and fission play a critical role in

80 proteins have been implicated in controlling mitochondrial fusion and fission processes in both livin

81 nd mtDNA depletion as well as aberrations of mitochondrial fusion and fission proteins, which eventua

82 We will address the ability of mitochondrial fusion and fission to impact all cell type

83 Although mitochondrial fusion and fission were dispensable for mt

84 he same cells, while variable alterations in mitochondrial fusion and fission were seen.

85 alterations of the opposing forces governing mitochondrial fusion and fission, similarly affect retin

86 of BCL2-like proteins may be as couplers of mitochondrial fusion and fission.

87 east, flies, and mammals are known to affect mitochondrial fusion and function.

88 on of mitofusin via HUWE1, thereby promoting mitochondrial fusion and function.

89 es mitofusin 2 (Mfn2), a protein involved in mitochondrial fusion and in tethering of mitochondria to

90 s in Drp1 mutants are suppressed by reducing mitochondrial fusion and increasing cytoplasmic ROS in s

91 Thus, OMM protein distribution depends on mitochondrial fusion and is a locus of apoptotic dysfunc

92 Our findings highlight a critical role for mitochondrial fusion and lipid homeostasis in GSC mainte

93 We propose a tenet that mitochondrial fusion and lipid metabolism are tightly li

94 two mammalian mitofusin GTPases that promote mitochondrial fusion and maintain organelle integrity.

95 (OPA1), a dynamin-like GTPase that regulates mitochondrial fusion and maintenance of cristae architec

96 s partially rescued by mutants that regulate mitochondrial fusion and maintenance of the tubular morp

97 MFN2 has two functions: it promotes inter-mitochondrial fusion and mediates endoplasmic reticulum

98 r four additional months, DNA methylation of mitochondrial fusion and mismatch repair proteins, Mfn2

99 results shed light on the molecular basis of mitochondrial fusion and mitofusin-related human neuromu

100 two opposing processes: bud-tip anchorage by mitochondrial fusion and Mmr1p, which favors bulk inheri

101 Thus, the separate functions of NME3 in mitochondrial fusion and NDP kinase cooperate in metabol

102 uced OMA1 activation and OPA1 cleavage limit mitochondrial fusion and promote neuronal death.

103 nomer restores homeostasis via autophagy and mitochondrial fusion and promotes basal tearing.

104 related to human SLP2, a protein involved in mitochondrial fusion and protein complex formation in th

105 complex disassembly via CHCHD10, and impairs mitochondrial fusion and respiration, phenotypes that ar

106 complexes in brain, associated with impaired mitochondrial fusion and respiration.

107 These inhibitors also suppress mitochondrial fusion and respiratory defects in IBMPFD p

108 control levels attenuated the htau-enhanced mitochondrial fusion and restored the functions, while d

109 Mitochondrial fusion and structure depend on the dynamin

110 so found increased mitochondrial biogenesis, mitochondrial fusion and synaptic activity and reduced m

111 damental insight into how mitofusins mediate mitochondrial fusion and the ways their disruptions caus

112 the metalloprotease OMA1, to prevent extreme mitochondrial fusion and to maintain optimal mitochondri

113 sociated regulatory factor), is required for mitochondrial fusion and transport in long axons.

114 ase associated MFN2 proteins suppressed both mitochondrial fusion and transport, and produced classic

115 nnection, mitofusin 2 (Mfn2) participates in mitochondrial fusion and undergoes repression in muscle

116 tic vesicle cycling, glutamate transmission, mitochondrial fusion, and calcium buffering, is complex

117 tin, increased mitochondrial mass, increased mitochondrial fusion, and increased PGC1alpha expression

118 ndrial permeability transition pore (mtPTP), mitochondrial fusion, and mtDNA biogenesis have already

119 The chronic inhibition of mitochondrial fusion as a result of genetic mutation is

120 an impaired mRNA export is not dependent on mitochondrial fusion, as the deletion of FZO1, an essent

121 By combining an in vitro mitochondrial fusion assay with electron cryo-tomography

122 Using a mitochondrial fusion assay, we established that L-OPA1 c

123 rane fusion DRPs using an in vitro mammalian mitochondrial fusion assay.

124 1 (OPA1) is a dynamin protein that mediates mitochondrial fusion at the inner membrane.

125 e results highlight the importance of normal mitochondrial fusion balance, as influenced by the OPA1

126 ls of fission genes, and increased levels of mitochondrial fusion, biogenesis and synaptic genes in S

127 phatidylethanolamine is proposed to regulate mitochondrial fusion, but its mechanism of action is unk

128 that the Mdm30-Ubp2-Rsp5 crosstalk regulates mitochondrial fusion by coordinating an intricate balanc

129 ammalian Phospholipase D MitoPLD facilitates mitochondrial fusion by generating the signaling lipid p

130 Impairing mitochondrial fusion by knocking down mitofusion-2 (Mfn2

131 elegans has previously been shown to promote mitochondrial fusion by physically interacting with the

132 inactive cytoplasmic Smad2 rapidly promotes mitochondrial fusion by recruiting RIN1 into a complex w

133 demonstrate that mitochondrial PE regulates mitochondrial fusion by regulating the biophysical prope

134 ns, and demonstrate that mitofusin-dependent mitochondrial fusion can be regulated in mouse cells by

135 Interruption of mitochondrial fusion causes lethal cardiac failure at a

136 ts that could be rescued by treatment with a mitochondrial fusion compound.

137 Interestingly, impairing mitochondrial fusion decreased OXPHOS but did not deplet

138 This suggests that the mitochondrial fusion defect in the Deltapsd1 strain coul

139 tochondrial fusion, further exacerbating the mitochondrial fusion defect of the Deltapsd1 strain.

140 s interconnected mitochondrial network and a mitochondrial fusion defect that is not explained by alt

141 ecies are key mediators of cardiomyopathy in mitochondrial fusion-defective cardiomyocytes.

142 Model and analyze mitochondrial fusion defects in Drosophila melanogaster

143 Surprisingly, a defect in maternal mitochondrial fusion delays PME, which is reversed by a

144 d regulation of dynamic properties including mitochondrial fusion, division, and transport.

145 the deletion of FZO1, an essential gene for mitochondrial fusion, does not alter the export of ADH1,

146 ed and aggregated mitochondria with impaired mitochondrial fusion during mating.

147 lated by cytoplasmic lipases, autophagy, and mitochondrial fusion dynamics, ensuring maximum oxidativ

148 In addition, mitochondrial fusion/dynamics were compromised in Ptpmt1

149 smic reticulum (ER) shape in addition to its mitochondrial fusion effects.

150 udies reveal that Mfn1, a GTPase involved in mitochondrial fusion, establishes a mitochondrial size t

151 he mitochondrial ATP pool via a shift toward mitochondrial fusion, excess mitochondrial reactive oxyg

152 otic Bcl2 protein, Bax, positively regulates mitochondrial fusion exclusively through homotypic MFN2

153 ondrial assembly regulatory factor (Marf), a mitochondrial fusion factor (mitofusin), as well as othe

154 ssociated Gp78 ubiquitin ligase and the Mfn1 mitochondrial fusion factor in mitophagy.

155 dependent degradation of the mitofusin (Mfn) mitochondrial fusion factors Mfn1/Mfn2.

156 48 h in Caenorhabditis elegans, and requires mitochondrial fusion, fission and autophagy, providing g

157 'Mitochondrial dynamics', the processes of mitochondrial fusion, fission, biogenesis and mitophagy

158 chondrial dysfunction with marked changes in mitochondrial fusion, fission, morphology and transcript

159 discuss the reciprocal interactions between mitochondrial fusion, fission, transport and mitophagy.

160 l dynamics, incorporating recent findings on mitochondrial fusion, fission, transport and mitophagy.

161 Mitochondrial fusion-fission cycles ensure independent g

162 zed a mouse model carrying a knockout of the mitochondrial fusion-fission-related gene solute carrier

163 bscured details of morphological dynamics of mitochondrial fusion/fission and ER remodeling, as well

164 on-defective mitochondrial size decreases, a mitochondrial fusion/fission cycle in adult mouse hearts

165 ng that alpha-syn operates downstream of the mitochondrial fusion/fission machinery.

166 In contrast, key players in mitochondrial fusion/fission or biogenesis were not sign

167 Here, we review newly described functions of mitochondrial fusion/fission proteins in cardiac mitocho

168 pro-fusion effect by increasing the ratio of mitochondrial fusion/fission proteins without resulting

169 The factors that couple mitochondrial fusion/fission with bioenergetics and thei

170 arance of damaged mitochondria by autophagy, mitochondrial fusion/fission, and biogenesis) may contri

171 in organelle division, viral resistance, and mitochondrial fusion/fission.

172 iogenesis of s-Mgm1, a protein essential for mitochondrial fusion, further exacerbating the mitochond

173 Remarkably, concomitant deletion of the mitochondrial fusion gene Mfn1 completely rescued heart

174 Increased synaptic and mitochondrial fusion genes and decreased fission genes w

175 (fission 1) and decreased expression of the mitochondrial fusion genes Mfn1 (mitofusin 1), Mfn2 (mit

176 cently emerged, implicating mutations in the mitochondrial fusion genes OPA1 and MFN2 in the pathogen

177 ommonly caused by mutations in the canonical mitochondrial fusion genes OPA1 and MFN2, respectively.

178 ress resistance, we found that disruption of mitochondrial fusion genes resulted in the upregulation

179 ructure in aged cells through control of the mitochondrial fusion GTPase Fzo1.

180 However, the function of s-OPA1 in mitochondrial fusion has been debated, because in some s

181 Mitochondrial fusion has not been observed in postmitoti

182 Cells deficient in mitochondrial fusion have been shown to have defects lin

183 i) verapamil suppressed both contraction and mitochondrial fusion, (ii) after spontaneous contraction

184 ochondrial fission and rescued by decreasing mitochondrial fusion, implying that mitochondria can phy

185 Mitochondrial fusion in adult cardiac myocytes is necess

186 However, the role of mitochondrial fusion in AEC2 function and lung fibrosis

187 that mutant SOD1 motor neurons have impaired mitochondrial fusion in axons and cell bodies.

188 Both forms of Bax restore mitochondrial fusion in Bax/Bak-null cells, which otherw

189 Here we report a role for mitochondrial fusion in bud-tip anchorage of mitochondri

190 rs describe how insulin signalling regulates mitochondrial fusion in C. elegans, and show that mitoch

191 SCF(LIN-23)-regulated pathway that controls mitochondrial fusion in Caenorhabditis elegans by repres

192 e BCL-2-like protein CED-9 in the control of mitochondrial fusion in Caenorhabditis elegans.

193 ons from pcd mice, and we documented reduced mitochondrial fusion in cells lacking CCP1.

194 Here we examine the functions of mitochondrial fusion in differentiated skeletal muscle t

195 The role of mitochondrial fusion in functioning of the heart, where

196 in breast cancer, is a pivotal regulator of mitochondrial fusion in glucose-starved cancer cells.

197 to promptly restore cellular metabolism and mitochondrial fusion in keeping with the short residence

198 ndrial membrane protein that participates in mitochondrial fusion in mammalian cells, contributes to

199 Suppressing cardiomyocyte mitochondrial fusion in Parkin-deficient fly heart tubes

200 ochondrial biogenesis in patient muscle, and mitochondrial fusion in patient fibroblasts associated w

201 Visualizing mitochondrial fusion in real time, we identified two cla

202 ional modification responsible for unopposed mitochondrial fusion in response to low glucose conditio

203 This pathway is required for mitochondrial fusion in response to physical exertion, a

204 rough FZO-1/Mfn1,2 and EAT-3/Opa1 to promote mitochondrial fusion in response to specific cellular si

205 ll identify how diet-dependent modulation of mitochondrial fusion in specific neuronal circuits impac

206 morphology, demonstrating a central role for mitochondrial fusion in the cardiomyopathy provoked by i

207 al ATP production in POMC neurons, promoting mitochondrial fusion in their neurites, and increasing P

208 Long OPA1 forms were sufficient to mediate mitochondrial fusion in these cells.

209 ysis of mitochondrial structure in cells and mitochondrial fusion in vitro, we found that conversion

210 with increased C18:0 dietary intake boosting mitochondrial fusion in vivo.

211 d organ function of disrupting cardiomyocyte mitochondrial fusion in vivo.

212 s not yet been possible to directly modulate mitochondrial fusion, in part because the structural bas

213 Suppressing mitochondrial fusion increased compensatory expression o

214 ent increased Opa-1 protein levels, promoted mitochondrial fusion, increased mitochondrial membrane p

215 Thus, mitochondrial fusion is an essential and direct target o

216 The increased mitochondrial fusion is essential for longevity in the d

217 Mitochondrial fusion is essential for maintenance of mit

218 Mitochondrial fusion is essential to cardiomyocyte mitoc

219 When mitochondrial fusion is genetically attenuated, the York

220 We examined whether mitochondrial fusion is important for metabolic tailorin

221 ing mtDNA function in the face of mutations, mitochondrial fusion is likely to be a protective factor

222 animals and yeasts, in which CL's effect on mitochondrial fusion is more profound, Arabidopsis CL pl

223 hondrial fusion in C. elegans, and show that mitochondrial fusion is necessary, but not sufficient, f

224 Our results suggest that increased mitochondrial fusion is not a major driver of longevity,

225 CED-9-induced mitochondrial fusion is not required for the maintenance

226 a provide insights into the pathway by which mitochondrial fusion is regulated in the cell.

227 We previously demonstrated that mitochondrial fusion is required for germline stem cell

228 tors of mitochondrial dynamics revealed that mitochondrial fusion is required for the maintenance of

229 t, in which mitochondrial fission occurs but mitochondrial fusion is restricted, suggesting that ced-

230 Mitochondrial fusion is thought to be important for supp

231 ns Mfn1 and Mfn2, large GTPases that mediate mitochondrial fusion, is induced by Parkin upon membrane

232 hondria from diverse eukaryotes, followed by mitochondrial fusion (limited mechanistically to green p

233 e metabolically altered and characterized by mitochondrial fusion, lipid accumulation, and reduced mi

234 Formation of lamellar cristae depends on the mitochondrial fusion machinery through a pathway that is

235 ion of Opa-1 and mitofusins, proteins of the mitochondrial fusion machinery, is dramatically altered

236 Multiple measures indicate that the mitochondrial fusion machinery, Mitofusins, accumulate a

237 er membrane protein Ugo1, a component of the mitochondrial fusion machinery.

238 hosphorylation-stimulated degradation of the mitochondrial fusion machinery.

239 ion phenotype, neither overexpression of the mitochondrial fusion/MAM-tethering protein MFN2 nor inhi

240 Interfering with mitochondrial fusion mechanisms in Agrp neurons by cell-

241 The expression of genes involved in mitochondrial fusion (Mfn1, Opa1) and fission (Drp1, Fis

242 Thus, attenuated mitochondrial fusion might contribute to the pathogenesi

243 HG-1 forms complexes with known mediators of mitochondrial fusion-mitofusins (Mfns) 1 and 2-and enhan

244 s and anoxia, surprisingly we found that the mitochondrial fusion mutants eat-3 and fzo-1 are more re

245 While both mitochondrial fission and mitochondrial fusion mutants showed increased sensitivit

246 phology observed in a drp-1 mutant, in which mitochondrial fusion occurs but mitochondrial fission is

247 Mitochondrial fusion occurs in many eukaryotes, includin

248 demonstrate that CED-9 can promote complete mitochondrial fusion of both the outer and inner mitocho

249 To directly test the effect of reduced mitochondrial fusion on hepatic metabolism, we generated

250 ut instead had a dominant negative effect on mitochondrial fusion only when MFN1 was at low levels, a

251 lished role of mitofusins (MFN1 and MFN2) in mitochondrial fusion, only MFN2 has been associated with

252 a within migrating cells by interfering with mitochondrial fusion (opa-1) or fission (drp-1) proteins

253 hrough a mechanism that depends on increased mitochondrial fusion, Opa-1, and the Akt-mTOR-NFkappaB p

254 cells was not associated with inhibition of mitochondrial fusion or bioenergetic defects, supporting

255 ivo mouse models in which mitofusin-mediated mitochondrial fusion or dynamin-related protein 1-mediat

256 Defects in mitochondrial fusion or fission are associated with many

257 several disease models, the manipulation of mitochondrial fusion or fission can partially rescue dis

258 cellular context, BCL2-like proteins promote mitochondrial fusion or fission.

259 with the highest mitochondrial ATP output), mitochondrial fusion, oxygen consumption, and Ca(2+) upt

260 Enhancing mitochondrial fusion partially rescued dendritic abnorma

261 We show that the mitochondrial fusion-promoting factor Drosophila Mitofus

262 p97 acts by targeting the mitochondrial fusion-promoting factor mitofusin for degr

263 her levels of total and active Drp1 and less mitochondrial fusion protein 1 (Mfn1).

264 al fusion by physically interacting with the mitochondrial fusion protein FZO-1.

265 ndrial fission activity or inhibition of the mitochondrial fusion protein Marf-1 in posterior-localiz

266 Importantly, co-expression of mitochondrial fusion protein mitofusin 2 (Mfn2) could ab

267 Elimination of the mitochondrial fusion protein mitofusin 2 (Mfn2) sensitiz

268 monstrates that a phosphorylated form of the mitochondrial fusion protein Mitofusin 2 serves as a rec

269 Here, we examine the role of the mitochondrial fusion protein optic atrophy 1 (OPA1) in d

270 Here we report that OPA1, a mitochondrial fusion protein, was hyperacetylated in hea

271 f lipid mixing and the biogenesis of Mgm1, a mitochondrial fusion protein.

272 mitochondrial trafficking adaptors, and the mitochondrial fusion proteins (mitofusins).

273 Concomitant decrease in mitochondrial fusion proteins and increased fission prot

274 se that induces degradation of the mitofusin mitochondrial fusion proteins and mitochondrial fission.

275 he recently discovered multifunctionality of mitochondrial fusion proteins and newly defined mechanis

276 MPP cleavage sites are also present in other mitochondrial fusion proteins from fungi, plants, and an

277 experiments indicate a fundamental role for mitochondrial fusion proteins in mammalian physiology.

278 Despite normal or increased levels of mitochondrial fusion proteins in mtPE-deficient cells, a

279 Transfection of HL-1 cells with the mitochondrial fusion proteins mitofusin 1 or 2 or with D

280 Here we report that the absence of the mitochondrial fusion proteins mitofusin1 (MFN1) and mito

281 he diverse longevity pathways, as inhibiting mitochondrial fusion reduces their lifespans to wild-typ

282 nd significantly decreased expression of the mitochondrial fusion related protein MFN1.

283 sturbances in mitochondrial architecture and mitochondrial fusion-related genes are observed in situa

284 ever, the mechanism by which lipids regulate mitochondrial fusion remains poorly understood.

285 Mitochondrial fusion requires the coordinated fusion of

286 tively controls mRNA export independently of mitochondrial fusion, revealing a novel function of an F

287 lated experiment, we find that disruption of mitochondrial fusion strongly increases mitochondrial dy

288 ptional up-regulation of genes that regulate mitochondrial fusion, such as opa1-like (opa1) and mitoc

289 m reveals a central mechanism that regulates mitochondrial fusion, the manipulation of which can corr

290 nd oxidized glutathione (GSSG) and initiated mitochondrial fusion through the coordinated action of M

291 on GTPase dynamin-related protein 1 promoted mitochondrial fusion, thus coupling mitochondrial energe

292 or to mitosis, but neither chloroplastic nor mitochondrial fusion took place, suggesting that these f

293 In contrast, disruption of mitochondrial fusion via knockdown of the inner mitochon

294 ix-targeted photoactivatable GFP showed that mitochondrial fusion was not inhibited in patient fibrob

295 When mitochondrial fusion was prevented in starved cells, FAs

296 expression, which plays an essential role in mitochondrial fusion, was observed in TDP-43PrP mice.

297 e mitofusins Mfn1 and Mfn2 are essential for mitochondrial fusion, we deleted these genes from a subs

298 eneration via enhancing mitofusin-associated mitochondrial fusion, which provides new insights into t

299 By contrast, depletion of Opa1 suppressed mitochondrial fusion while sparing transport, and did no

300 ochondrial fragmentation and a lower rate of mitochondrial fusion, while ELMOD2 overexpression promot