ライフサイエンスコーパス: growth cone

1 dynamics for reorganization at the neuronal growth cone.

2 ft and the invasion of microtubules into the growth cone.

3 morphogenesis and filopodia formation in the growth cone.

4 nel and the Galphaq signaling pathway at the growth cone.

5 and Rab4 contribute to recycling within the growth cone.

6 the entire length of the axon, including the growth cone.

7 the repertoire of receptors available on the growth cone.

8 microtubule dynamics and organization in the growth cone.

9 pulling by an actin-driven mechanism in the growth cone.

10 ulation increases phospho-ZBP1 levels in the growth cone.

11 s the local translation of beta-actin at the growth cone.

12 slation of proteins, including actin, in the growth cone.

13 erentiation via cytoskeletal dynamics in the growth cone.

14 hasic bi-directional turning response of the growth cone.

15 levels ofGAP43mRNA and protein in axons and growth cones.

16 ed filopodia from mouse dorsal root ganglion growth cones.

17 ns of sensory neurons in vitro, primarily in growth cones.

18 upts local protein synthesis within neuronal growth cones.

19 argets of the ubiquitin-proteasome system in growth cones.

20 thematical model of membrane polarization in growth cones.

21 ise modulation of biochemical signals within growth cones.

22 erns of membrane dynamics in rat hippocampal growth cones.

23 nthesis and degradation are linked events in growth cones.

24 in, in lamellipodia and filopodia of Aplysia growth cones.

25 ression in sub-cytoplasmic locations such as growth cones.

26 nd dynamics are regulated by Src in neuronal growth cones.

27 specific signaling mechanisms that occur in growth cones.

28 ading edges of migrating neurons and neurite growth cones.

29 n of GAP43 suffices for efficient sorting to growth cones.

30 d in colorectal cancer (DCC), on sympathetic growth cones.

31 tin and inhibited filopodium mobility in the growth cones.

32 tion of Frizzled3 in rodent commissural axon growth cones.

33 of SPAG6 affected the growth of neurites and growth cones.

34 ng development by motile structures known as growth cones.

35 d a disruption of actin dynamics in neuronal growth cones.

36 ncreased localization of p35 to neurites and growth cones.

37 ch the guidance cues either attract or repel growth cones.

38 critical early during regeneration to direct growth cones across the transection gap and onto their o

39 is linked by dDAAM to the regulation of the growth cone actin cytoskeleton, and thereby growth cone

40 nd the role of the actin nucleator Arp2/3 in growth cone actin dynamics and guidance.

41 toskeleton and apCAM substrates, stimulating growth cone advance if sufficiently abundant.

42 vel of traction force did not correlate with growth cone advance toward the adhesion site, but the am

43 In cases of adhesion-mediated growth cone advance, the mean needle deflection was 1.05

44 roneedles coated with apCAM ligands to guide growth cone advance.

45 e microtubule-rich region at the rear of the growth cone and along the axon has never, to our knowled

46 easure force generation over the rear of the growth cone and along the axon of chick sensory neurons.

47 dual mechanism: by directly signaling at the growth cone and by regulating the processing of other re

48 gulation of microtubule dynamics in the axon growth cone and enhances our understanding of this proce

49 n the ability of cut CNS axons to form a new growth cone and then elongate.

50 ositive endosomes via Rab4 occurs within the growth cone and thereby supports axon elongation.

51 KBP) as critical for SCG10 transport to axon growth cones and complete axon extension.

52 al protein degradation is a major feature of growth cones and creates a requirement for local transla

53 nal protein that regulates actin dynamics in growth cones and facilitates axonal growth.

54 ation of filopodial protrusion in developing growth cones and for inhibition of growth cone filopodia

55 netrin-1, p120RasGAP is recruited to DCC in growth cones and forms a multiprotein complex with focal

56 tner and showed that radixin accumulation in growth cones and its LPA-dependent phosphorylation depen

57 MP1, restoresGAP43mRNA and protein levels in growth cones and rescues axon outgrowth defects in SMA n

58 pontaneous transients of local exocytosis in growth cones and that these transients are positively re

59 reduced USP9X protein localization in axonal growth cones, and (in 2/3 variants) failed to rescue neu

60 e-rich neuronal structures such as axons and growth cones, and can interact with membranes both via i

61 d solely during axon extension, localized to growth cones, and essential for axon outgrowth; however,

62 SP preceding filopodia formation in neuronal growth cones, and uncover a molecular heterogeneity wher

63 Microtubule dynamics at the growth cone are mediated by alpha7 nicotinic receptor ac

64 Growth cones are attracted to intermediate targets, but

65 During neural circuit assembly, axonal growth cones are exposed to multiple guidance signals at

66 growth cone behaviors.SIGNIFICANCE STATEMENT Growth cones are the motile tips of growing axons whose

67 action force in Aplysia californica neuronal growth cones as they develop over time in response to a

68 e fly DLK Wallenda (Wnd) in R7 photoreceptor growth cones as they halt at their targets and become pr

69 t IGF-1 receptor activation is important for growth cone assembly and axonal formation.

70 nisms leading to the formation of dystrophic growth cone at the injured axonal tip, the subsequent ax

71 Receptors on the growth cone at the leading edge of elongating axons play

72 Navigation of the growth cone at the tip of the developing axon is crucial

73 MET is heavily expressed in neuronal growth cones at early developmental stages and its activ

74 opment depends on the proper balance of axon growth cone attractive and repellent cues leading axons

75 However, as R7 growth cones become boutons, Wnd levels are further repr

76 growth cone actin cytoskeleton, and thereby growth cone behavior, in a direct way.

77 rotubule (MT) cytoskeleton are essential for growth cone behaviors during axon growth and guidance.

78 ytoskeletal organization and dynamics during growth cone behaviors.SIGNIFICANCE STATEMENT Growth cone

79 ance cues play a central role in controlling growth cone behaviour.

80 by disrupting the net assembly of MTs at the growth cone, but rather because it alters the balance of

81 proteins, which, among others, reorient RGC growth cones by regulating intracellular second messenge

82 Both approaches showed that Aplysia growth cones can develop traction forces in the 10(0)-10

83 g tau expression disrupts MT bundling in the growth cone central domain, misdirects trajectories of M

84 in orthogonal protrusions emanating from the growth cone central domain.

85 laevis spinal neurons selectively abolished growth cone chemorepulsion but permitted chemoattraction

86 rs targeted by the ISNb nerve, as well as at growth cone choice points and synaptic targets for the I

87 ling destabilizes microtubules to facilitate growth cone collapse and axon termination.

88 ence microscopy, and cell-based and neuronal growth cone collapse assays.

89 of EphA3 was essential for ephrin-A5-induced growth cone collapse in cortical GABAergic interneurons,

90 rotein that is essential for proBDNF-induced growth cone collapse in developing dopaminergic processe

91 ibits RGC neurite outgrowth and enhances RGC growth cone collapse in response to exogenous ephrinA5 l

92 activity and mediates neurite retraction and growth cone collapse in response to repulsive guidance c

93 These findings provide insight into how growth cone collapse is regulated during axon terminatio

94 resent, relatively little is known about how growth cone collapse occurs prior to axon termination in

95 Growth cone collapse prior to termination is facilitated

96 Given the prominence of the cytoskeleton in growth cone collapse, we assessed the relationship betwe

97 dation of RhoA, a mediator of Sema3A-induced growth cone collapse.

98 ein-synthesis requirement for Sema3A-induced growth cone collapse.

99 use frontal cortex through ephrin-A5-induced growth cone collapse.

100 eing able to block Sema3A chemorepulsion and growth-cone collapse in axons at the extracellular level

101 re able to inhibit endogenous EphA4-mediated growth-cone collapse induced by ephrin-B3.

102 ations of Dscam1 phosphorylation in distinct growth-cone compartments enable the spatial specificity

103 of full-length UNC-5::GFP and UNC-40::GFP in growth cones, consistent with a model in which UNC-73, U

104 with Hermes knock-down resulting in aberrant growth cone cue sensitivity and axonal topographic mispr

105 anism of how Shh orchestrates changes in the growth cone cytoskeleton that are required for growth co

106 How Shh elicits changes in the growth cone cytoskeleton that drive growth cone turning

107 the organization and dynamics of the axonal growth cone cytoskeleton.

108 ificantly lower (0.48 +/- 0.06 mum) when the growth cones did not advance.

109 However, how the growth cone differs from other non-neural cells remains

110 Nogo receptors (NgR1, NgR2, and NgR3) are growth cone directive molecules known for inhibiting axo

111 Delivery of proteins and organelles to the growth cone during axon extension relies on anterograde

112 Hence, growth cone dynamics can influence wiring specificity wi

113 tinuous, fast and high-resolution imaging of growth cone dynamics from axon growth to synapse formati

114 Our approach combines intravital imaging of growth cone dynamics in developing brains of intact pupa

115 th cone guidance, but the types and roles of growth cone dynamics underlying neural circuit assembly

116 onent of the multiprotein complex regulating growth cone dynamics.

117 em cell proliferation, radial migration, and growth cone dynamics.

118 sport is essential for maintenance of axonal growth-cone dynamics and autophagosome turnover.

119 r, our study provides the best evidence that growth cone-ECM adhesions clutch RF locally to guide axo

120 g, such as retraction of neurites and axonal growth cones, elevated neuronal rigidity, and reshaping

121 or division stall in the proximal nerve; the growth cones enlarge, extend excessive filopodia, and as

122 mulation increases beta-actin protein at the growth cone even when the cell bodies have been removed.

123 We find that growth cones exhibit high levels of ubiquitination and t

124 mutants lacking Schwann cells, regenerating growth cones extend at rates comparable with wild type y

125 o a reduction in the number of filopodia and growth cone F-actin content on laminin and L1.

126 anosine triphosphatases within the extending growth cone facilitates the dynamic reorganization of th

127 vents single dynamic MTs from extending into growth cone filopodia along actin filament bundles.

128 down of Actbeta reduces dynamic movements of growth cone filopodia and impairs presynaptic differenti

129 Neuronal growth cone filopodia contain guidance receptors and con

130 ing development, we examined the behavior of growth cone filopodia during the exploration of both cor

131 neurons as a model we show that >90% of the growth cone filopodia exhibit fast, stochastic dynamics

132 We examined embryonic growth cone filopodia in vivo to directly observe their

133 rite length, (2) neurite complexity, and (3) growth cone filopodia number, in accordance with CD2AP e

134 substrata elicit local Ca(2+) signals within growth cone filopodia that regulate axon guidance throug

135 lization of endogenous adhesion signaling to growth cone filopodia.

136 NC-44 influence cytoskeletal function during growth cone filopodial inhibition.

137 ive UNC-40/DCC receptor signaling stimulates growth cone filopodial protrusion and that repulsive UNC

138 eveloping growth cones and for inhibition of growth cone filopodial protrusion caused by activated MY

139 roscopy to show how Drosophila photoreceptor growth cones find their targets.

140 Analysis of growth cone forces applied to beads at low stiffness of

141 Here, we show that neuronal growth cones form protrusions that share molecular, stru

142 of function in rsks-1 results in more rapid growth cone formation after injury and accelerates subse

143 both of which are required for regenerative growth cone formation, and which act downstream of EFA-6

144 Growth cones from all neuron types and species examined,

145 We found that newly formed growth cones from axons re-emerging from an axonal injur

146 1 effectors LIMK1 and cofilin was reduced in growth cones from NCAM-deficient neurons, which was acco

147 ificant increase of the well known marker of growth cones, GAP-43; and an enhancement of endoplasmic

148 key event of cytoskeleton remodeling in the growth cone (GC) during axon outgrowth and pathfinding.

149 as a cell adhesion molecule (CAM) in axonal growth cones (GCs) of the developing brain.

150 We find the rear of the growth cone generates 2.0 nN of contractile force, the a

151 maphorins were initially described as axonal growth cone guidance molecules that signal through plexi

152 Microtubules are also important in growth cone guidance, because their polarized invasion i

153 Filopodial dynamics are thought to control growth cone guidance, but the types and roles of growth

154 e of Frizzled3 recycling in PCP signaling in growth cone guidance.

155 by the PHR protein Highwire (Hiw) during R7 growth cone halting, as has been observed in other syste

156 DLK levels are regulated within a developing growth cone has not been examined.

157 c molecules involved in recycling within the growth cone have not been fully characterized.

158 n cell morphology reverses once regenerating growth cones have crossed the injury site and have grown

159 f PDL and LN, we demonstrate that individual growth cones have differential RF rates while interactin

160 Single-growth-cone imaging reveals that Slit/RPTP69D are not re

161 ar to retrograde actin flow in lamellipodia, growth cones, immunological synapses, dendritic spines,

162 Axon guidance is driven by changes in the growth cone in response to gradients of guidance molecul

163 As in other animals, axon growth cones in Caenorhabditis elegans integrate informa

164 ster cells and (b) the dynamic properties of growth cones in catecholaminergic a-differentiated neuro

165 mature axon terminals as well as at immature growth cones in response to microglia-derived signals, w

166 r, lead to differential positioning of their growth cones in the early target region.

167 een used to direct the outgrowth on neuronal growth cones, indicating a therapeutic potential for neu

168 Sensory trigeminal growth cones innervate the cornea in a coordinated fashi

169 how NGF elicits faster axon outgrowth or how growth cones integrate and transform signal input to mot

170 Growth cones interact with the extracellular matrix (ECM

171 t PTPsigma has a critical role in converting growth cones into a dystrophic state by tightly stabiliz

172 Growth cone invadosomes contain dynamic F-actin and seve

173 The nerve growth cone is bi-directionally attracted and repelled b

174 nto the peripheral domain on one side of the growth cone is essential for it to turn in that directio

175 h order dependent pre-patterning of afferent growth cones is an essential pre-requisite for the ident

176 One important signal that controls growth cones is that of local Ca(2+) transients, which c

177 Although actin at neuronal growth cones is well-studied, much less is known about a

178 However, in growth cones, it is unclear whether similar F-actin-clut

179 reduced levels of SCG10 in kbp(st23) mutant growth cones led to altered microtubule stability, defin

180 decompaction; these effects are dependent on growth cone localization of Hmgn5 mRNA.

181 Here we demonstrate that UNC-45A is a novel growth cone--localized, NMII-associated component of the

182 d CLIP-170 form F-actin-dependent patches in growth cones, mediated by binding of the coiled-coil dom

183 Our findings suggest that Kv3.4 reduces growth cone membrane excitability and maintains [Ca(2+)]

184 pening of Kv3.4 channels effectively reduces growth cone membrane excitability, thereby limiting exce

185 adhesion molecules (IgCAMs) to the neuronal growth cone membrane through its ability to control the

186 Since growth cones migrate in association with diverse adhesiv

187 ected role for a Notum homolog in regulating growth cone migration, separate from the well establishe

188 sensing and provide the force necessary for growth cone migration.

189 l mitochondria are specifically required for growth-cone migration, identifying a key energy challeng

190 ed selection process is well explained by a 'growth-cone' model, which selects surface elements in an

191 zation in the optic chiasm and tract and RGC growth cone morphologies are also altered in Dscam mutan

192 phorylation of Mena/VASP proteins as well as growth cone morphology and neurite outgrowth.

193 cient mutant of radixin did not fully rescue growth cone morphology and switched netrin tropism from

194 ssion of wild-type radixin partially rescued growth cone morphology and tropism toward netrin in ERM-

195 ated in the regulation of neurite length and growth cone morphology.

196 ted neurite outgrowth, branch formation, and growth cone morphology.

197 ic insight into Ca(2+)/calpain regulation of growth cone motility and axon guidance during neuronal d

198 Dual leucine zipper kinase (DLK) promotes growth cone motility and must be restrained to ensure no

199 d motility, which are fundamental for proper growth cone motility and neurite extension.

200 a model in which Src and cortactin regulate growth cone motility by increasing actin network density

201 aps that of other actin binding proteins, in growth cone motility is substrate dependent.

202 However, how calpain regulates growth cone motility remains unclear.

203 tracellular signaling mechanisms that govern growth cone motility will clarify how the nervous system

204 we found substrate-dependent differences in growth cone motility, actin retrograde flow, and guidanc

205 n guidance that mediates opposing effects on growth cone motility.

206 Neuronal growth cones move forward by dynamically connecting acti

207 y measurements of the detailed statistics of growth cone movements in both attractive and repulsive g

208 actin-cross-linking proteins at the neuronal growth cone, namely phosphorylated Ezrin/Radixin/Moesin.

209 direct modulation of MTs by guidance cues in growth cone navigation but also help us to understand mo

210 P1 and LRP2 ligands for the ability to guide growth cone navigation.

211 with endocrine cells and at the neuron soma, growth cones, neurites, axons, and dendrites but not at

212 id, protein synthesis-dependent increases in growth cone NFPC and its cofactor, TAF1, in vitro.

213 Neither actin filaments in the growth cone nor tubulin polymerization is required for i

214 ing to IP3 receptor (IP3R) activation at the growth cone of differentiating PC12 cells.

215 wiring during development requires that the growth cones of axons and dendrites are correctly guided

216 MGN5) chromatin binding protein localizes to growth cones of both neuron-like cells and of hippocampa

217 synaptic vesicle clusters present at axonal growth cones of developing neurons.

218 activate ephrinB signaling and collapse the growth cones of distant neurons.

219 at Kv3.4, the major Kv channel in the axonal growth cones of embryonic dorsal spinal neurons, is acti

220 Membrane excitability in the axonal growth cones of embryonic neurons influences axon growth

221 report that Kv3.4 is expressed in the axonal growth cones of embryonic spinal commissural neurons, mo

222 which is transiently expressed in the axonal growth cones of many types of embryonic neurons, acts to

223 Moreover, the growth cones of primary small-diameter dorsal root gangl

224 We demonstrate here that growth cones of temporal axons collapse when contacting

225 rons that RF is reduced in rapidly migrating growth cones on laminin (LN) compared with non-integrin-

226 Growth cones on neuronal process navigate over long dist

227 in a crowded brain region despite extensive growth cone overlaps and provides a framework for matchi

228 n in the rate of microtubule invasion of the growth cone (P<0.001).

229 ork that occurs during axonal elongation and growth-cone pauses arises because strong contractile for

230 estored MT bundling, MT penetration into the growth cone periphery and close MT apposition to actin f

231 ssion, depleted dynamic microtubules and the growth cone periphery, and impaired neuron migration.

232 referentially to dynamic microtubules in the growth cone periphery.

233 nd microtubule exploration of the actin-rich growth cone periphery.

234 gulation of microtubule (MT) dynamics in the growth cone plays an important role in axon guidance.

235 One presumed function of growth cone point contacts is to restrain or "clutch" my

236 Further, we show that the initial growth cone positioning determines synaptic layer select

237 This initial growth cone positioning is consolidated via cell-adhesio

238 -associated protein 43 (GAP43), a well known growth cone protein that promotes axonal regeneration, c

239 strong contractile forces in the rear of the growth cone pull material forward.

240 We report that, in growth cones, Rab5 and Rab4 proteins localize to endosom

241 localization to dynamic microtubules within growth cones, rather than adjacent axonal microtubule bu

242 After axotomy, neuronal survival and growth cone re-formation are required for axon regenerat

243 Overexpression of DCLK2 accelerated growth cone re-formation in vitro and enhanced the initi

244 sing live imaging, we show, however, that R8 growth cones reach and recognize their target without Ne

245 involves extrinsic molecular cues that bind growth cone receptors and signal to the cytoskeleton thr

246 robust enhancement of axon regeneration and growth cone reformation.

247 n have been identified, membrane dynamics in growth cones remains largely unknown.

248 Because glia and glial-derived growth cone repellent factors (especially the diffusible

249 heses that Nogo receptors are membrane-bound growth cone repellent factors required for migration of

250 phorylation and RhoA signaling necessary for growth cone repulsion in GABAergic interneurons in vitro

251 ngly, we found no qualitative differences in growth cone response or axon growth, suggesting that, de

252 ion to replenish proteins needed to maintain growth cone responses.

253 nt manner and that Netrin-ephrin synergistic growth cones responses involve the potentiation of Src f

254 or ligand-dependent p75(NTR) activation in a growth cone retraction functional assay.

255 l adaptation assays demonstrate that retinal growth cones robustly adapt towards ephrin-A/EphA forwar

256 transcription factor Sequoia regulate R cell growth cone segregation.

257 lly, we find such 'co-adaptation' in retinal growth cones specifically for ephrin-A/EphA signaling.

258 ngth, which in turn controls axon growth and growth cone sprouting.

259 n controls both fast filopodial dynamics and growth cone stabilization.

260 Correspondingly, R7 growth cones stabilize early and change their final posi

261 Mechanisms of actin-dependent growth cone steering, via signaling cascades, are well d

262 5 endosomes and move to the periphery of the growth cone, suggesting that both Rab5 and Rab4 contribu

263 5 and Rab4 are recruited to endosomes in the growth cone, suggesting that they control recycling loca

264 we show for the first time in living axonal growth cones that tau is important for microtubule bundl

265 zation in mesenchymal cells but not neuronal growth cones, thus displaying cell-type specificity.

266 ubstrates applied to the surface of neuronal growth cones to characterize the development of forces e

267 ues modulate the peripheral actin network in growth cones to direct axons to their targets.

268 imary targeting defects, but destabilizes R7 growth cones to jump between correct and incorrect layer

269 The sensitivity of growth cones to semaphorin 3F and Eph receptor B2, two r

270 site was insufficient to direct regenerating growth cones toward the original path, providing compell

271 However, in vitro, growth cones trace highly stochastic trajectories, and e

272 oduces the most accurate predictive model of growth cone trajectories to date, and deepens our unders

273 to axon termination is protracted, with the growth cone transitioning from a dynamic to a static sta

274 etric profile of the bead target and forward growth cone translocation; pharmacological inhibition of

275 ng effects on RF rates were also observed in growth cones treated with chemoattractive and chemorepul

276 nsory neurons (rat dorsal root ganglia) in a growth cone turning assay, we tested a range of LRP1 and

277 , which was then experimentally confirmed by growth cone turning assays and Ca(2+) imaging.

278 hat tau knockdown reduced axon outgrowth and growth cone turning in Wnt5a gradients, likely due to di

279 s in the growth cone cytoskeleton that drive growth cone turning is unknown.

280 Local protein synthesis directs growth cone turning of nascent axons, but mechanisms gov

281 tly tau knockdown reduced axon outgrowth and growth cone turning, due to disorganized microtubules th

282 ch signaling cascades can potentially affect growth cone turning, namely through regulatable forces i

283 n modulates both basal neurite outgrowth and growth cone turning.

284 hibition of MS TRPC1 is sufficient to induce growth cone turning.

285 owth cone cytoskeleton that are required for growth cone turning.

286 Taken together, our results suggest that growth cones use invadosomes to target protease activity

287 oskeletal proteins at the ventral surface of growth cones using single particle tracking combined to

288 The traction force exerted by the growth cone was measured by monitoring the microneedle d

289 , using super resolution microscopy of fixed growth cones, we found that tau colocalizes with MTs and

290 tiotemporal dynamics of protein synthesis in growth cones, we further developed a technique for singl

291 activity of Pak1 were enhanced when isolated growth cones were incubated with NCAM function triggerin

292 e Drosophila visual system, R8 photoreceptor growth cones were shown to require Net-Fra to reach thei

293 ion, we found that RF rates of spinal neuron growth cones were slower in vivo than what was observed

294 s stimulate actin polymerization in neuronal growth cones whereas repulsive cues induce actin disasse

295 s SynI mobilization at presynaptic sites and growth cones, whereas the use of inhibitors of sphingoli

296 Membrane excitability in the growth cone, which is mainly controlled by voltage-gated

297 gradients provide critical signals to guide growth cones, which are the motile tips of developing ax

298 Transplanted hMDSPCs surrounded the axonal growth cone, while hMDSPCs infiltrating the regenerating

299 Arp2/3 to the plasma membrane, resulting in growth cones with deficient actin veils in stem cell-der

300 c-75 or its targets, regenerating axons form growth cones, yet are deficient in extension.