ライフサイエンスコーパス: growth cone

1 indicative of an aberrant composition of the growth cone.

2 dynamics for reorganization at the neuronal growth cone.

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

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

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

6 erentiation via cytoskeletal dynamics in the growth cone.

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

8 vant sites, such as the motor neuron and the growth cone.

9 atial localization of actin in the advancing growth cone.

10 e dynamic filopodial domain that defines the growth cone.

11 r cues that activate receptors on the axonal growth cone.

12 ciated phenotypic nuance at the scale of the growth cone.

13 ique expression profiles of molecules on the growth cone.

14 n both lamellipodia and filopodia of Aplysia growth cones.

15 ise modulation of biochemical signals within growth cones.

16 tion of Frizzled3 in rodent commissural axon growth cones.

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

18 ng development by motile structures known as growth cones.

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

20 ncreased localization of p35 to neurites and growth cones.

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

22 levels ofGAP43mRNA and protein in axons and growth cones.

23 ed filopodia from mouse dorsal root ganglion growth cones.

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

25 upts local protein synthesis within neuronal growth cones.

26 w presynaptic terminals and scattered axonal growth cones.

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

28 thematical model of membrane polarization in growth cones.

29 f lamellipodia in migrating cells and axonal growth cones.

30 ents to localize calcium signals in steering growth cones.

31 otubules, within filopodia, thereby steering growth cones.

32 ER remodeling to the motile side of steering growth cones.

33 egment, in the axon shaft, at synapses or in growth cones.

34 e and subsequent ER remodeling in navigating growth cones.

35 ch Abl biases the stochastic fluctuations of growth cone actin to direct axon growth and guidance.

36 onin (5-HT) is known to increase the rate of growth cone advance via cofilin-dependent increases in r

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

38 To overcome these limitations, we developed Growth Cone Analyzer (GCA).

39 rganization and distribution of actin in the growth cone and are coupled to growth cone velocity.

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

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

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

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

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

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

46 During development, neurons form growth cones and neurites, but later reduce these activi

47 typically regulate the motility of neuronal growth cones and other migrating cell types by acting as

48 nockdown nearly eliminates branched actin in growth cones and prevents growth cone recovery after rep

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

50 e show that STIM1 associates with EB1/EB3 in growth cones and that STIM1 expression is critical for m

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

52 to accumulation of activated Ret in pioneer growth cones, and reduced retrograde Ret51 transport.

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

54 The core morphological features of the growth cone are strongly correlated with one another and

55 Growth cones are attracted to intermediate targets, but

56 Growth cones are complex, motile structures at the tip o

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

58 ells, the functions of cortactin in neuronal growth cones are not well understood.

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

60 n in neurite outgrowth and a 60% increase in growth cone area already 24 hours after plating; axonal

61 ptic-like vesicles accumulate in the central growth cone as the pioneer axon breaches the spinal boun

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

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

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

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

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

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

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

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

70 We propose that nestin changes growth cone behavior by regulating intracellular kinase

71 We propose that nestin changes growth cone behavior by regulating the intracellular kin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 cue Semaphorin3a (Sema3a), leading to axonal growth cone collapse in vitro.

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

88 by triggering a reduction of p-Cofilin-S3, a growth cone collapse marker, through decreasing a novel

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

90 Growth cone collapse prior to termination is facilitated

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

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

93 quired for dendrite elaboration but not axon growth cone collapse.

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

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

96 However, it is unknown whether and how the growth cones communicate with each other while sensing a

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

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

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

100 localization of calcium signals controls the growth cone cytoskeleton to direct motility.

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

102 gnal transduction pathway that regulates the growth cone cytoskeleton.

103 T1 is essential for BDNF-stimulated neuronal growth cone development and dendritic protrusion formati

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

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

106 ulate cytoskeletal reorganization within the growth cone direct axon navigation.

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

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

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

110 range retrograde Ret signaling in regulating growth cone dynamics through downstream transcriptional

111 onent of the multiprotein complex regulating growth cone dynamics.

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

113 sulted in abnormal dendritic protrusions and growth cone dynamics.

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

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

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

117 e mechanism by which SlitC constantly limits growth cone exploration, imposing ordered and forward-di

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

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

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

121 nal myosin Myo16 in cortical neurons altered growth cone filopodia density and axonal branching patte

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

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

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

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

126 ndent manner, whereas localization of MTs to growth cone filopodia was facilitated by direct MT bindi

127 lization of endogenous adhesion signaling to growth cone filopodia.

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

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

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

131 CGH-1 results in increased axon regrowth and growth cone formation, whereas loss of DCAP-1 or DCAP-2

132 The long-held view is that Slits push growth cones forward and prevent them from turning back

133 Growth cones from all neuron types and species examined,

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

135 Growth cones from either LRRK2 knockout or G2019S knocki

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

137 The growth cone (GC) itself can generate very low intracellu

138 on between the MT and actin cytoskeletons in growth cones (GCs) during axon guidance.

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

140 ur findings demonstrate that LRRK2 regulates growth cone-growth cone communication in axon guidance a

141 kinase 2 (LRRK2), has an unexpected role in growth cone-growth cone communication.

142 Cs in the fly is schizo and its loss affects growth cone guidance at the midline in the CNS, also an

143 These data demonstrate that intrinsic growth cone guidance machinery can be co-opted to non-in

144 a photoactivatable Rac1 to co-opt endogenous growth cone guidance machinery to precisely and non-inva

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

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

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

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

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

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

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

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

153 ocalization of calcium signals in navigating growth cones in the nascent nervous system.

154 and reveal molecular specializations of the growth cone, including accumulations of the growth-regul

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

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

157 Growth cones interact with the extracellular matrix (ECM

158 CK1delta mutants, neurons continue to sprout growth cones into adulthood, leading to a highly ramifie

159 We find that the growth cone is almost purely filopodial, and that it ext

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

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

162 he spatial distribution of Vangl2 within the growth cone is selectively affected by an N-cadherin-coa

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

164 regulation of calcium signaling in neuronal growth cones is essential for axon guidance.

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

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

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

168 ation induces local Ca(2+) transients at the growth cone, leading to activation of nitric oxide synth

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

170 on speed and for the dynamic organization of growth-cone-like branch tips.

171 cheal sprouts invade IFMs directionally with growth-cone-like structures at branch tips.

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

173 nally, loss of Ret reduced transcription and growth cone localization of Myosin-X, an initiator of fi

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

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

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

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

178 c points in axon navigation as regulators of growth cone microenvironment.

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

180 uggesting multiple functions of STIM1 within growth cones (Mitchell et al., 2012).

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

182 GCA is designed to quantify growth cone morphodynamics from time-lapse sequences ima

183 actin organization and its consequences for growth cone morphogenesis and motility.

184 adaptability of GCA through the analysis of growth cone morphological variation and its relation to

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

186 displayed defects in peripheral sensory axon growth cone morphology and dynamics.

187 O mice to show that the effects of nestin on growth cone morphology and on Sema3a sensitivity are DCX

188 ied in developing neurons where it regulates growth cone morphology and responsiveness to the guidanc

189 molecular mechanism by which nestin affects growth cone morphology and Sema3a sensitivity.

190 Changes in growth cone morphology require rearrangements of cytoske

191 Changes in growth cone morphology require rearrangements of cytoske

192 g cortical cultures, nestin regulates axonal growth cone morphology.

193 ting axonal growth and retraction as well as growth cone morphology.

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

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

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

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

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

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

200 dulates the cytoskeleton to produce directed growth cone motility.

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

202 dulates the cytoskeleton to produce directed growth cone motility.

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

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

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

206 orting cells located along the trajectory of growth cone navigation.

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

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

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

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

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

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

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

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

215 microtubule tips toward the leading edge in growth cones of hippocampal neurons.

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

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

218 l transcriptomes and proteomes from labelled growth cones of single projections in vivo.

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

220 Growth cones on neuronal process navigate over long dist

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

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

223 Filopodia at the growth cone periphery have long been considered sensors

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

225 In growth cones, Pfn1 increased actin retrograde flow, MT g

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

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

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

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

230 tive analysis reveals two separate groups of growth cone properties that together account for growth

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

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

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

234 branched actin in growth cones and prevents growth cone recovery after repellent-induced collapse.

235 d molecular enrichments in trans-hemispheric growth cones relative to their parent cell bodies, produ

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

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

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

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

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

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

242 a Met-rich receptor that initiates neuronal growth cone retraction.

243 Both p75(NTR) forms support proNT-induced growth cone retraction: We show that receptor surface ac

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

245 transcription factor Sequoia regulate R cell growth cone segregation.

246 form specific connections, here we developed growth cone sorting and subcellular RNA-proteome mapping

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

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

249 r neuroscience such as, mechanistically, how growth cones stall and how axonal microtubules resist fo

250 However, STIM1 is also required for growth cone steering away from semaphorin-3a, a guidance

251 eracting molecule 1 (STIM1) is necessary for growth cone steering toward the calcium-dependent guidan

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

253 th cone properties that together account for growth cone structure and dynamics.

254 Each projection is formed by growth cones-subcellular specializations at the tips of

255 that nestin-expressing neurons have smaller growth cones, suggesting that nestin affects cytoskeleta

256 vestigate the set of molecules within native growth cones that form specific connections, here we dev

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

258 In growth cones, the endoplasmic reticulum (ER) is a signif

259 a6 causes an increase of explorative MTs: in growth cones they enhance axon growth, in axon shafts th

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

261 sic, stochastic fluctuations of actin in the growth cone to produce axon growth and guidance.

262 counter a concentration gradient that causes growth cones to become dystrophic and axons to retract o

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

264 in trans to modulate the response of axonal growth cones to soluble gradients to selectively orchest

265 uidance cues act during development to guide growth cones to their proper targets in both the central

266 eries of impenetrable barriers, forcing axon growth cones to traverse one half of each somite as they

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

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

269 Following axon pathfinding, growth cones transition from stochastic filopodial explo

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

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

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

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

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

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

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

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

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

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

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

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

282 rojection within and away from the organoid, growth-cone turning, and decussation.

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

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

285 Here we show that Vangl2 controls growth cone velocity by regulating the internal retrogra

286 actin in the growth cone and are coupled to growth cone velocity.

287 II that is spatiotemporally regulated in the growth cone via mechanocatalytic effects to modulate neu

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

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

293 , transcripts are transported along axons to growth cones, where they are rapidly translated in respo

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 thus of the dynamic filopodial domain of the growth cone, while maintaining the essential coherence o

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.