ライフサイエンスコーパス: cristae

1 and invaginations toward the matrix, called cristae.

2 cated on the folded inner membrane, known as cristae.

3 s along the highly curved ridges of lamellar cristae.

4 sponsible for generating the helical tubular cristae.

5 M/TOB) complex and controls the shape of the cristae.

6 ad to the generation of lamellar and tubular cristae.

7 with abnormalities in shapes and numbers of cristae.

8 s have morphologies similar to mitochondrial cristae.

9 ding loss, disorganization and dilatation of cristae.

10 nect the inner boundary membrane to lamellar cristae.

11 l and peripheral zones in semicircular canal cristae.

12 x of subunit 4 lack both dimers and lamellar cristae.

13 e on an enlarged appearance with reorganized cristae.

14 ion of highly curved ridges in mitochondrial cristae.

15 membrane and the inner membrane with folded cristae.

16 mal mitochondrial matrix and packed lamellar cristae.

17 membrane proteins that control the shapes of cristae.

18 l-x(L) also localized to inner mitochondrial cristae.

19 ria are swollen and many have no discernible cristae.

20 plete absence of the semicircular canals and cristae.

21 itochondria and remodeling the mitochondrial cristae.

22 semicircular canals, anterior and posterior cristae.

23 circular canals and their associated sensory cristae.

24 the formation of vesicle germination-derived cristae.

25 ral (CZ) and peripheral (PZ) zones of monkey cristae.

26 he mitochondrial inner matrix, and disrupted cristae.

27 of the mitochondrial matrix and swelling of cristae.

28 ocalized predominantly to organized lamellar cristae.

29 onomer interface that occur in mitochondrial cristae.

30 h is insufficient to visualize mitochondrial cristae.

31 DeltaPsi(m) at the resolution of individual cristae.

32 ng ribbons at the rims of the inner membrane cristae.

33 s indicate how they shape the inner membrane cristae.

34 closely resemble those in the inner membrane cristae.

35 the perpendicular alignment of mitochondrial cristae.

36 chondrial morphology with a loss of internal cristae.

37 cated on the folded inner membrane, known as cristae.

38 not entirely clear why mitochondria develop cristae?

39 , displayed fragmented mitochondria with few cristae, a less-polarized mitochondrial membrane potenti

40 hat L-OPA1 cleavage is a novel mechanism for cristae abnormalities because of both C10 mutation and C

41 and Tfam as well as mitochondrial volume and cristae abundance were significantly higher with (-)-epi

42 Vestibular tissues (cristae ampullares, macular otolithic organs, and Scarpa

43 input for rotary head movements (detected by cristae ampullaris) and not by loss of input for linear

44 the vasculature throughout the stroma of the cristae ampullaris, the maculae utricle, and saccule in

45 crystalline inclusions, ii) linearization of cristae and abnormal angular features, iii) concentric l

46 w swelling of mitochondria with disorganized cristae and areas of condensation.

47 ins that maintain the connection between the cristae and boundary membranes.

48 ered structural changes in the mitochondrial cristae and caused increased fragmentation by blocking m

49 We discovered the polarization of cristae and crista junctions in mitochondria tethered to

50 Our results show disorganized mitochondrial cristae and degenerating mitochondria in endothelial cel

51 l mitochondria that were devoid of organized cristae and displayed severe membrane abnormalities.

52 cently demonstrated that S-OPA1 can maintain cristae and energetics through its GTPase activity, desp

53 with distinct DeltaPsi(m) , corresponding to cristae and IBM.

54 , disrupt complex I activity, or destabilize cristae and inhibit NADH-dependent respiration.

55 mitochondrial membrane (IMM), consisting of cristae and inner boundary membranes (IBM), is considere

56 etformin triggers the disorganization of the cristae and inner mitochondrial membrane in several canc

57 hifts through the parallel remodeling of the cristae and of the MERCs via a mechanism that degrades O

58 ia, which are fragmented, display remodelled cristae and release cytochrome c, thereby driving apopto

59 o cleave OPA1 resulting in remodeling of the cristae and release of the highly concentrated protons w

60 e absence of Aim24 leads to complete loss of cristae and respiratory complexes.

61 rtion of COX proteins, was also localized to cristae and reticular structures isolated in the matrix

62 ons passed through cartilages, cartilaginous cristae and ridges on the plantar side of the distal tib

63 embranes failed to form tubular or vesicular cristae and showed as closely packed stacks of membrane

64 OPA1 is also necessary for maintaining the cristae and thus essential for supporting cellular energ

65 mechanoreceptor organs, the utricle/saccule, cristae, and cochlea, with distinct types of acellular m

66 hondrial network fragmentation, disorganised cristae, and increased autophagosomes.

67 ) skeletal muscle were swollen with abnormal cristae, and mitochondrial biogenesis was increased.

68 th fragmented and tubular cristae or loss of cristae, and reduced crista membrane.

69 a strikingly altered ultrastructure, lack of cristae, and swelling.

70 ed by large invaginations, the mitochondrial cristae, and the inner boundary membrane, which is in pr

71 ug on mitochondria viz. disruption of normal cristae architecture and dissipation of mitochondrial tr

72 Miro2 are required for normal mitochondrial cristae architecture and Endoplasmic Reticulum-Mitochond

73 Consistent with OPA1 maintaining cristae architecture, its down-regulation resulted in EM

74 ates mitochondrial fusion and maintenance of cristae architecture.

75 Instead, cristae are either absent or balloon-shaped, with ATP sy

76 Tubular cristae are formed via invaginations of the inner bounda

77 plexes of oxidative phosphorylation, but how cristae are formed, remained an open question.

78 strongly impaired and irregular, and stacked cristae are present.

79 These IMJs and associated cristae arrays may provide the structural basis to enhan

80 ctural changes transitioning from glycolytic cristae at E8.5, to more traditional mitochondria at E10

81 coordination of inner mitochondrial membrane cristae at inter-mitochondrial junctions (IMJs).

82 C2/C10 DKO mice have disrupted mitochondrial cristae, because of cleavage of the mitochondrial-shapin

83 A), caused by mutations in the mitochondrial cristae biogenesis and fusion protein optic atrophy 1 (O

84 Opa1), a mitochondrial GTPase that regulates cristae biogenesis and mitochondria dynamics.

85 (HCs) in squirrel monkey (Saimiri sciureus) cristae by a nearly 3:1 ratio.

86 a-reperfusion injury, protects mitochondrial cristae by interacting with cardiolipin on the inner mit

87 nthase dimers and ATP production in inflated cristae by mitofilin down-regulation concomitant to MICO

88 by improving the structure of mitochondrial cristae, can increase the oxidative phosphorylation rate

89 O Journal, Wolf et al (2019) report that the cristae carry a higher membrane potential than the inter

90 sed of the outer and inner membranes and the cristae cluster, which enclosed the lower density mitoch

91 DeltaPsi(m) was higher at cristae compared to IBM.

92 ternal mitochondrial membranes invagination (cristae) complexity was calculated by the mitochondrial

93 Mitochondrial cristae contain electron transport chain complexes and a

94 nic bioenergetics level: 1) The formation of cristae creates more mitochondrial inner membrane surfac

95 analysis revealed swollen mitochondria with cristae damage in the kdsr(I105R) mutant hepatocytes, wh

96 QIL1 expression rescued cristae defects, and promoted re-accumulation of MICOS s

97 Here, we demonstrate that cristae-deficient mitochondria (mitosomes) of Trachiplei

98 ts down-regulation resulted in EM-detectable cristae deformity.

99 enriched fibres have significantly increased cristae density and that, at the whole-body level, muscl

100 indings establish an elevating mitochondrial cristae density as a regulatory mechanism for increasing

101 engages, the mitochondria network fragments, cristae density drops by 30%, and mitochondrial respirat

102 te dehydrogenase histochemical activity, and cristae density increased.

103 t the whole-body level, muscle mitochondrial cristae density is a better predictor of maximal oxygen

104 trast to the current view, the mitochondrial cristae density is not constant but, instead, exhibits p

105 Intramitochondrial cristae density of synGLT-1 KO mice was increased, sugge

106 spirations, ATP synthesis, and mitochondrial cristae density were decreased in cardiac mitochondria a

107 on per mitochondria depends on plasticity in cristae density, although current evidence for such a me

108 ondrial rupture, decreased mitochondrial and cristae density, release of cytochrome C and apoptosis i

109 Formation of lamellar cristae depends on the mitochondrial fusion machinery th

110 ostatic pressure for 3 days induced abnormal cristae depletion and decreased the length of the mitoch

111 ntially reduced cristae volume, and abnormal cristae depletion in 10-month-old glaucomatous ONH axons

112 reduction of COX, mitochondrial fission and cristae depletion, alterations of OPA1 and Dnm1 expressi

113 re triggered mitochondrial fission, abnormal cristae depletion, Drp-1 translocation, and cellular ATP

114 e to normal, mitochondrial fragmentation and cristae destruction were evident, and mitochondrial area

115 With increasing age, the typical cristae disappear and the inner membrane vesiculates.

116 rated pericytes displaying mitochondria with cristae disruption, 3) degenerated astrocytes and periva

117 The forms of the cristae during mitochondrial fusion and fission can be c

118 n it binds to CL-containing membranes in the cristae early in apoptosis.

119 xic adaptation is reported as rounding sharp cristae edges and expanding cristae width (ICS) by parti

120 ATP synthase dimers determine sharp cristae edges, whereas trimeric OPA1 tightens ICS outlet

121 risingly, short cilia form in mechanosensory cristae even in the absence of kif3a In contrast to Kif3

122 and FAO, while fission in TE cells leads to cristae expansion, reducing ETC efficiency and promoting

123 s the IMM surface is large, due to extensive cristae folding.

124 se cytochrome c is mostly sequestered within cristae folds but released rapidly and completely during

125 proximately 15 nm, the size of mitochondrial cristae folds.

126 They are required for cristae formation and a main factor in mitochondrial mor

127 COS assembly, mitochondrial respiration, and cristae formation critical for mitochondrial architectur

128 r structure explains the structural basis of cristae formation in mitochondria, a landmark signature

129 One proposed role of cristae formation is to facilitate the establishment of

130 Mic60 is an ancient mechanism, important for cristae formation, and had already evolved before alpha-

131 mination and membrane invagination models of cristae formation.

132 tion preserves mitochondrial respiration and cristae formation.

133 animals had abnormal neuronal mitochondrial cristae formation.

134 mitochondrial membrane that is required for cristae formation.

135 with a smaller adipocyte size and increased cristae formation.

136 n, which is required for dimer stability and cristae formation.

137 ic units, preventing the failure of specific cristae from spreading dysfunction to the rest.

138 Our experiments reveal that, in developing cristae, hair cells stratify into an upper, Tmc2a-depend

139 he biological significance for mitochondrial cristae has now, for the first time, been elucidated at

140 echanism by which they disrupt mitochondrial cristae, however, has been uncertain.

141 ructurally damaged mitochondria, with broken cristae in AbetaPP primary neurons.

142 The mitochondrial cristae in CHCM1/CHCHD6-deficient cells become hollow wi

143 hy to characterize the formation of lamellar cristae in immature mitochondria during a period of dram

144 tudy the dynamic structures of mitochondrial cristae in live cells with a superresolution technique.

145 In mammalian skeletal muscle, the density of cristae in mitochondria is assumed to be constant.

146 tra-structural defects and loss of organized cristae in mitochondria of the Polg2(-/-) embryos as wel

147 ion and activation of CaMK-II in maculae and cristae in older embryos suggests continued roles in aud

148 oosely packed and disorganized mitochondrial cristae in TGiPLA2gamma mice that were accompanied by de

149 was reduced to 50% suggesting remodeling of cristae in the absence of ChChd3.

150 OPA1 localizes to mitochondrial cristae in the inner membrane where electron transport c

151 FM labeling of lateral cristae in tmc double mutants revealed the presence of t

152 d mitochondrial density and size and loss of cristae) in WT, but not kin(-) cells.

153 tivity, increased supercomplexes, and denser cristae, independent of mitochondrial biogenesis.

154 ry (inner boundary membrane) than inside the cristae, indicating high accessibility to cytosol-derive

155 We postulate that FGFs in the cristae induce a canal genesis zone by inducing/upregula

156 3D-reconstruction revealed the highly folded cristae inner membrane, features of functionally active

157 The segmentation to visualize the cristae invaginations into the mitochondrial matrix was

158 f the highly concentrated protons within the cristae invaginations.

159 Furthermore, unfolding of inner membrane cristae is coupled to changes in the supramolecular asse

160 The structural integrity of mitochondrial cristae is crucial for mitochondrial functions; however,

161 The mitochondrial contact site and cristae junction (CJ) organizing system (MICOS) dynamica

162 lex distribution, and thus, potentially also cristae junction copy number.

163 by narrow, tubular membrane segments called cristae junctions (CJs).

164 MICOS subcomplexes independently localize to cristae junctions and are connected via Mic19, which fun

165 unit complex that localizes to mitochondrial cristae junctions and organizes cristae positioning with

166 e mitochondrial mitofilin protein complex at cristae junctions in patient fibroblasts bearing the CHC

167 phenomenon of largely horizontally arranged cristae junctions that connect the inner boundary membra

168 se in inner:outer membrane ratio, whereas no cristae junctions were detected.

169 d in the intermembrane space and enriched at cristae junctions.

170 INOS subunit, is preferentially localized at cristae junctions.

171 cted over the inner membrane in wild type or cristae-lacking cells.

172 karyotic membranes, induces the formation of cristae-like plasma membrane invaginations.

173 ril degeneration, disorganized mitochondrial cristae, lipid inclusions and vacuolation.

174 vivo functions of Mgm1, membrane fusion and cristae maintenance, and more generally shed light onto

175 s in mitochondrial inner membrane fusion and cristae maintenance.

176 We hypothesize that some lamellar cristae may be organized by a vesicle germination proces

177 the inner membrane, implying that individual cristae may operate with some degree of independence.

178 omains of the contiguous inner membrane--the cristae membrane (CM) and the inner boundary membrane (I

179 and required for the establishment of normal cristae membrane architecture.

180 lar or slit-like structures that connect the cristae membrane with the inner boundary membrane, there

181 TP synthase is more centrally located at the cristae membrane.

182 ria that connect the inner boundary with the cristae membrane.

183 e oxidative phosphorylation complexes in the cristae membranes assists kinetic coupling between proto

184 Pretreatment of rats with SS-31 protected cristae membranes during renal ischemia and prevented mi

185 wever, sequestration of OXPHOS components in cristae membranes necessitates a re-examination of the e

186 because ischemia destroys the mitochondrial cristae membranes required for mitochondrial ATP synthes

187 d mitochondria that were virtually devoid of cristae membranes, demonstrating the importance of these

188 ngular features, iii) concentric layering of cristae membranes, iv) matrix compartmentalization, v) n

189 t mitochondrial abnormalities, mostly in the cristae membranes.

190 uced Ca(2+) uptake, and marked plasticity of cristae membranes.

191 associated with MICOS disassembly, abnormal cristae, mild cytochrome c oxidase defect, and sensitivi

192 titative morphological parameter to evaluate cristae modelling and can be applied to compare healthy

193 Overall, our study elaborates on how cristae morphogenesis and functional maturation are intr

194 n of Oma1 restored mitochondrial tubulation, cristae morphogenesis, and apoptotic resistance in cells

195 drial protein named CHCM1 (coiled coil helix cristae morphology 1)/CHCHD6.

196 tion of the TOB/SAM complex leads to altered cristae morphology and a moderate reduction in the numbe

197 is a critical organizer of the mitochondrial cristae morphology and thus indispensable for normal mit

198 P synthase oligomer mutants, exhibit altered cristae morphology even though ATP synthase oligomer for

199 red during hypoxia, and we therefore studied cristae morphology in HepG2 cells adapted to 5% oxygen f

200 -ray tomography to characterize mitochondria cristae morphology isolated from murine.

201 ion of wild-type YME1L restored the lamellar cristae morphology of YME1L-deficient mitochondria.

202 MICOS assembly and cristae morphology were not efficiently rescued by over-

203 the mitochondrial inner membranes, regulates cristae morphology, and maintains respiratory chain func

204 e MICOS complex, necessary for CJ integrity, cristae morphology, and mitochondrial function and provi

205 HD6 is linked to regulation of mitochondrial cristae morphology, cell growth, ATP production, and oxy

206 liferation and apoptotic resistance, altered cristae morphology, diminished rotenone-sensitive respir

207 Our data suggest that, by altering cristae morphology, fusion in TM cells configures electr

208 itochondria and a fundamental determinant of cristae morphology.

209 ner membrane, crucial for the maintenance of cristae morphology.

210 which is known to also control mitochondrial cristae morphology.

211 kdown causes severe defects in mitochondrial cristae morphology.

212 ma-1 and immt-1 also have similar effects on cristae morphology.

213 iameter are an indirect effect of disrupting cristae morphology.

214 Mfn-knockdown flies also display altered cristae morphology.

215 of unknown function, controls mitochondrial cristae morphology.

216 ribution bands is largely independent of the cristae morphology.

217 itochondrial features, including conspicuous cristae, mtDNA, the tricarboxylic acid (TCA) cycle, and

218 A change in the shape of mitochondrial cristae must take place to attain rapid and complete rel

219 vacuolization, swelling, and dissolution of cristae occurred in axons as early as 3 days after sensi

220 At the associated junctions, the cristae of adjacent mitochondria form parallel arrays pe

221 Under fed ad libitum conditions, the cristae of mitochondria that apposed LD were mostly orga

222 which was absent in reduced or OMM-detached cristae of OPA1- and mitofilin-silenced cells, respectiv

223 completely absent in the apex and all three cristae of the semicircular canal ampullae.

224 eversed between vestibular hair cells in the cristae of the semicircular canals and auditory hair cel

225 The cristae of these fragmented mitochondria are disorganize

226 al membranes and the correct distribution of cristae on the mitochondrial membrane.

227 Remarkably, mitochondria and their cristae openings align with those of neighboring inner s

228 mbrane and often appear to be wrapped around cristae or crista-like inner membrane invaginations.

229 al IM structures with fragmented and tubular cristae or loss of cristae, and reduced crista membrane.

230 ial genome but do not preserve mitochondrial cristae or respiratory chain supercomplex assembly in pr

231 species, resistant to genetic disruption of cristae organization, dynamically modulated by mitochond

232 caspase (Smac), alteration of mitochondrial cristae organization, generation of reactive oxygen spec

233 hase, and the mitochondrial contact site and cristae organizing system (MICOS) complex.

234 Mic60) of the mitochondrial contact site and cristae organizing system (MICOS) IMM complex is attache

235 The mitochondrial contact site and cristae organizing system (MICOS) is a multisubunit prot

236 The mitochondrial contact site and cristae organizing system (MICOS) is a recently discover

237 multisubunit mitochondrial contact site and cristae organizing system (MICOS) was found to be a majo

238 onents of the mitochondrial contact site and cristae organizing system (MICOS), fully recapitulates t

239 ranes and the mitochondrial contact site and cristae organizing system (MICOS).

240 tion with the Mitochondrial Contact Site and Cristae Organizing System (MICOS).

241 contains the mitochondrial contact site and cristae organizing system 60-kD subunit, the translocase

242 the complex "mitochondrial contact site and cristae organizing system" and its subunits Mic10 to Mic

243 The MICOS (mitochondrial contact site and cristae organizing system) complex, crucial for proper a

244 ps2-Mdm35 and mitochondrial contact site and cristae organizing system, in the biosynthesis and trans

245 ced coexistence of tubular and flat lamellar cristae phases.

246 itochondrial cristae junctions and organizes cristae positioning within the organelle.

247 al integrity and biogenesis of mitochondrial cristae remain to be fully elucidated.

248 unds the role and mechanism of mitochondrial cristae remodeling in apoptosis.

249 n mitochondria-ER tethering, thereby linking cristae remodeling to MERC assembly.

250 ochrome c mobilization through Opa1-mediated cristae remodeling.

251 ated protein OPA1 are critical regulators of cristae remodeling.

252 ctor in mitochondrial homeostasis, including cristae remodeling; therefore, we examined the photorece

253 iting apoptosis as genetic interference with cristae remodelling and cytochrome c release.

254 r, OPA1, regulating inner membrane dynamics, cristae remodelling, oxidative phosphorylation, was post

255 ation factors generates concentric ring-like cristae, restores tubular mitochondrial morphology, and

256 Sectioned images of the cristae reveal that they have neither a baffle nor septa

257 rs are found in rows along the highly curved cristae ridges, and appear to be crucial for membrane mo

258 n promote neuronal survival independently of cristae shape, whereas stress-induced OMA1 activation an

259 meostasis proteins, fission-fusion proteins, cristae-shape controlling and MICOS proteins, and the co

260 of respiring mitochondrial networks through cristae stabilization, phosphorylation of chaperones and

261 hearts exhibited a distinctive mitochondrial cristae-stacking abnormality suggestive of a phospholipi

262 initial mitochondrial leak of OPA1 leads to cristae structural alterations and exposure of previousl

263 ced mitochondrial proton gradient, disrupted cristae structure and defective cardiolipin remodeling.

264 tructure are known, the relationship between cristae structure and function during organelle developm

265 ip of the inner mitochondrial membrane (IMM) cristae structure and intracristal space (ICS) to oxidat

266 ing a mitochondrial large GTPase involved in cristae structure and mitochondrial network fusion.

267 characterized for its role in mitochondrial cristae structure and organelle fusion, possible effects

268 Changes in mitochondrial cristae structure appeared from Day 3 highlighting the p

269 The cristae structure in the Opa1 (+/-) photoreceptors was n

270 Impairment of cristae structure through deletion of MICOS-complex comp

271 erations (i.e., enlargement, partial loss of cristae structure) and impairment of respiratory superco

272 ntermembrane space important for maintaining cristae structure, is co-released with cytochrome c.

273 S-OPA1 alone maintained normal mitochondrial cristae structure, which has been commonly assumed to be

274 for maintaining mitochondrial energetics and cristae structure.

275 c from mitochondria, in part by controlling cristae structures.

276 h invaginations of the inner membrane called cristae that contain the protein complexes of the oxidat

277 lateral otocyst into semicircular canals and cristae through two distinct mechanisms: regulating the

278 activity of OPA1 is critical for maintaining cristae tightness and thus energetic competency.

279 he ATP synthase dimers that form rows at the cristae tips dissociate into monomers in inner-membrane

280 key cellular structures (from mitochondrial cristae to nuclear pores) lie below the diffraction limi

281 The ratio of cristae to outer membrane surface area is large in these

282 ers of the helical arrays match those of the cristae tubes, suggesting the unique features of the P.

283 Unlike cristae, type II HCs predominate in monkey maculae.

284 it variable respiratory defects and abnormal cristae ultrastructure.

285 stical analysis of cryoelectron tomograms of cristae vesicles isolated from Drosophila flight-muscle

286 sion, matrix swelling, substantially reduced cristae volume, and abnormal cristae depletion in 10-mon

287 We found that the formation of lamellar cristae was associated with the gain of cytochrome c oxi

288 n the concave inner surface of mitochondrial cristae, we estimate the LPR of cardiolipin to cytochrom

289 More than 60 years ago, cristae were discovered as characteristic elements of mi

290 tomography showed some COX-positive lamellar cristae were not connected to IBM.

291 Matrix and cristae were retained but distributed unevenly with less

292 Presynaptic mitochondrial cristae were widened, suggesting a sustained energy dema

293 nanodomains originate from the mitochondrial cristae, which are compressed upon calcium signal propag

294 l expression in central zones of maculae and cristae, which are innervated by phasic neurons that are

295 show both forms to localize to mitochondrial cristae, which contain not only locally curved membranes

296 r boundary membrane and invaginations called cristae, which differ in protein composition and likely

297 causing acute depolarization may affect some cristae while sparing others.

298 s rounding sharp cristae edges and expanding cristae width (ICS) by partial mitofilin/Mic60 down-regu

299 Lastly, we determined that different cristae within the individual mitochondrion can have dis

300 ether, our data support a new model in which cristae within the same mitochondrion behave as independ