ライフサイエンスコーパス: otic

1 tometric open tubular ion chromatography (SC-OTIC).

2 nd 11 of 48 geniculate, 15 of 50 and 8 of 50 otic, 14 of 47 and 4 of 47 submandibular, 18 of 58 and 1

3 , low power consumption, and simplicity make OTIC a good candidate for such a mission.

4 s a relatively conserved pattern of the post-otic and a more variable morphology of the pre-otic cran

5 forkhead factor, Foxi1, is required for both otic and epibranchial placode development.

6 Mis-expression of Pax3 in the Pax2+ otic and epibranchial placodes also downregulates Pax2 a

7 However, we find that otic and epibranchial placodes form at different times a

8 ay essential roles in the differentiation of otic and olfactory neurons and their integration into th

9 ndant roles in the specification of the PPR, otic and olfactory placodes.

10 tion of the neural crest and placodes to the otic and olfactory systems.

11 ter stages, several sensory tissues (retina, otic, and olfactory epithelia) also expressed Kv2.2 prot

12 development in the trigeminal, epibranchial, otic, and olfactory placodes coincides with detachment o

13 Specification of the otic anteroposterior axis is one of the earliest pattern

14 ) and the abnormal deposition of bone at the otic capsule are common causes of conductive hearing imp

15 No evidence of otic capsule invasion was present in the remaining 31 ea

16 In addition, the size of the otic capsule is increased in Noggin -/- mutants, which m

17 cterized by abnormal bone remodelling in the otic capsule leading to fixation of the stapedial footpl

18 In contrast, induction of the otic capsule occurred normally demonstrating that induct

19 nerve relative to the parachordal plate, the otic capsules and the metotic fissure in gnathostomes.

20 differentiation of stem cell-generated human otic cell types.

21 In the absence of either N-cadherin or N-CAM otic cells lose apical cell-cell contact and their epith

22 mutants depleted of RA signaling produce few otic cells, and these cells fail to form a vesicle, indi

23 sure the transition of progenitors to mature otic cells, while simultaneously repressing alternative

24 er cells promote neurog1 expression in other otic cells.

25 In lia(-/-) (fgf3(-/-)) mutants, anterior otic character is reduced, but not lost altogether.

26 es in the gene regulatory network underlying otic commitment and reveal dynamic changes in gene expre

27 Thus, excess RA expands otic competence, whereas the loss of RA impairs the expr

28 ults confirm earlier descriptions of the pre-otic cranial nerves and present the first detailed descr

29 t the first detailed description of the post-otic cranial nerves.

30 ic and a more variable morphology of the pre-otic cranial nerves.

31 Ventral otic derivatives failed to form in Smo(ecko) embryos, wh

32 Consequently, ventral otic derivatives, including the cochlear duct and saccul

33 r duct and saccule, fail to form, and dorsal otic derivatives, including the semicircular canals, end

34 the gene regulatory network underlying early otic development by identifying direct inputs that media

35 However, the function of Rac GTPases in otic development is largely unexplored.

36 n during gastrulation can inhibit or promote otic development, depending on context, whereas misexpre

37 ling pathway is active at multiple stages of otic development, including during vestibular morphogene

38 (Fgf9) and sensory (Fgf20) epithelium during otic development, regulate the number of cochlear progen

39 ey instructional roles for MIF in vertebrate otic development.

40 nchial deficiencies but has little effect on otic development.

41 ration, cell death and cell movements during otic development.

42 ssion of foxi1, a necessary step for further otic development.

43 unction reveal that high levels of Pax favor otic differentiation whereas low levels increase cell nu

44 nstructs the high levels of Pax2a that favor otic differentiation.

45 cells can be continually recruited into the otic domain and uncover SPRY regulation of the size of a

46 stined to become cranial epidermis, into the otic domain.

47 We provide new morphologic data on otic dysmorphogenesis in Fgf3 mutants, which show a rang

48 Depletion of sp8 resulted in otic dysmorphogenesis, such as uncompartmentalized and e

49 pitulates Pax2 expression in the presumptive otic ectoderm.

50 uggested that Fgf initially induces a common otic/epibranchial field, which later subdivides in respo

51 naling, was conditionally inactivated in the otic epithelium (Smo(ecko)).

52 ls from the neural tube incorporate into the otic epithelium after otic placode induction has occurre

53 n the prospective neurosensory domain of the otic epithelium as morphogenesis initiates, is required

54 place of neuroblasts' delamination from the otic epithelium prefigure their position within the SAG.

55 Here we show that deletion of Rac1 in the otic epithelium resulted in severe defects in cochlear e

56 pioneer cells expressing neurog1 outside the otic epithelium that migrate and ingress into the epithe

57 fication defines the specific regions of the otic epithelium that will give rise to the six separate

58 ner ear, namely a strong contribution to the otic epithelium with the exception of sensory patches.

59 ins of Hoxa1 expression in rhombomere 3, the otic epithelium, and cardiac precursors, suggesting a mo

60 of sensorineural precursor cells within the otic epithelium, but is not expressed in migrating or pr

61 on and striking morphological changes in the otic epithelium, characterized by abnormal localization

62 and neurons overlap within the posteromedial otic epithelium.

63 of prosensory markers throughout the entire otic epithelium.

64 itory cells are regionally segregated in the otic epithelium.

65 lowing ectopic expression in chick embryonic otic epithelium.

66 Otic expression of extracellular matrix components is hi

67 Additionally, pax2/8 activate otic expression of fgf24, which induces epibranchial exp

68 th related genes pax2a/pax2b to downregulate otic expression of foxi1, a necessary step for further o

69 tially, Fgf from surrounding tissues induces otic expression of pax8 and sox3, which cooperate synerg

70 factor Pax2 plays a key role in coordinating otic fate and placode morphogenesis, but appears to regu

71 Specification towards otic fate requires diverse signals and transcriptional i

72 which cooperate synergistically to establish otic fate.

73 ompromising the induction and maintenance of otic fate.

74 Foxi1 provides competence to adopt an otic fate.

75 ink between FGF-induced formation of the pre-otic field and restriction of the otic placode to ectode

76 pression fail to be specified within the pre-otic field.

77 pterygopalatine, lingual, submandibular, and otic ganglia--arise from glial cells in nerves, not neur

78 ghlight the hierarchical organisation of the otic gene network.

79 o ways, by directly upregulating a subset of otic genes, and by positively regulating components of t

80 ecessary and sufficient to specify posterior otic identity between the 10 somite (otic placode) and 2

81 we demonstrate that ventral, but not dorsal, otic identity is directly dependent on Hh.

82 useful for reprogramming naive cells towards otic identity to restore hearing loss.

83 re-pattern to specify anterior and posterior otic identity, respectively.

84 ecessary and sufficient to specify posterior otic identity.

85 on molecules, it is not sufficient to confer otic identity.

86 d becoming ectoderm capable of responding to otic-inducing growth factors.

87 t Fgf8 is the primary factor responsible for otic induction in RA-depleted embryos.

88 f3, which is expressed in the hindbrain from otic induction through endolymphatic duct outgrowth, and

89 r otic induction, previous attempts to study otic induction through Fgf misexpression have yielded wi

90 Despite the vital importance of Fgf for otic induction, previous attempts to study otic inductio

91 e target genes suggested by other studies of otic induction.

92 and macrophages were recruited to localized otic infection with mutant and wild-type S. iniae and we

93 ly chimaeroid specializations, including the otic labyrinth arrangement and the brain space configura

94 icate atrial siphon primordia and posterior (otic, lateral line, and epibranchial) placodes of verteb

95 Otic lichen planus can lead to persistent hearing loss a

96 y recognition of the nonspecific symptoms of otic lichen planus may lead to prompt treatment and avoi

97 ay 31, 2011, of patients with a diagnosis of otic lichen planus.

98 l presentation, diagnosis, and management of otic lichen planus.

99 ed discrimination of non-neural ectoderm and otic lineage cells from off-target populations.

100 r development and for the segregation of the otic lineage from epibranchial progenitors.

101 lineate a developmental trajectory for human otic lineage specification in vitro.

102 al ectoderm, preplacodal ectoderm, and early otic lineage.

103 ence of Pax2, otic progenitors not only lose otic marker expression, but also fail to elongate due to

104 where FGF activity is favorable for PPR and otic marker expression.

105 asynchronous occurrences of preplacodal and otic marker genes.

106 d from different axial levels, to induce the otic marker Pax8 when recombined with blastula stage ani

107 ownstream factors Pax2a or Pax8 also expands otic markers but cannot bypass the requirement for Fgf o

108 Expression analysis of the known otic markers showed that Lmo4 is essential for the norma

109 ion after gastrulation leads to expansion of otic markers throughout preplacodal ectoderm surrounding

110 s to assay 96 genes representing established otic markers, signaling-pathway-associated transcripts,

111 pic otic vesicles expressing a full range of otic markers.

112 1, which is required for Fgf to expand other otic markers.

113 from the animal cap and express several pan-otic markers.

114 dicate that the composition of extracellular otic membranes is highly conserved between mammals and f

115 sults indicate a model whereby Pou3f4 in the otic mesenchyme establishes an Eph/ephrin-mediated fasci

116 of dense SGN fascicles that project through otic mesenchyme to form synapses within the cochlea.

117 isrupted when Pou3f4 (DFNX2) is deleted from otic mesenchyme.

118 BMP signaling for chondrogenesis in the peri-otic mesenchyme.

119 We show that post-otic migratory NC cells express RhoA, using RT-PCR on is

120 d comparisons with other mutations affecting otic morphogenesis, allow placement of Fgf3 between hind

121 he spatio-temporal migratory pattern of post-otic NC and the in vivo role of the small Rho GTPase, Rh

122 act disrupt the precise spatio-temporal post-otic NC cell migratory pattern.

123 in controlling Sox10 expression via a common otic/neural crest enhancer suggests an evolutionarily co

124 enetic mechanism controlling delamination of otic neuroblasts.

125 We propose a novel view for otic neurogenesis integrating cell dynamics whereby ingr

126 scription factor SOX2 has been implicated in otic neurogenesis, but its requirement in the specificat

127 to uncover the construction of the zebrafish otic neurogenic domain.

128 dels, we show that EYA1 and SIX1 are crucial otic neuronal determination factors upstream of NEUROG1

129 epithelialising placode to become the first otic neuronal progenitors.

130 t SOX2 is required for the initial events in otic neuronal specification including expression of NEUR

131 the otic placode dictates positional cues to otic neurons.

132 y to sensory organs and to the corresponding otic neurons.

133 nsplanted into an auditory neuropathy model, otic neuroprogenitors engraft, differentiate and signifi

134 tiated by WNT signaling that leads to dorsal otic patterning and endolymphatic duct formation.

135 ene Fgf10, by comparing different markers of otic patterning and hair cell differentiation.

136 ations had no major effects on expression of otic patterning genes or on cell survival, but resulted

137 The compartmentalized expression of otic patterning genes within the Rac1(CKO); Rac3(-/-) mu

138 oes not affect dorsoventral and mediolateral otic patterning, we now show that a gain of Hh signallin

139 h is predominantly required for dorsoventral otic patterning.

140 , from its initial onset in the invaginating otic placode and onwards throughout gestation, controlli

141 tivation of its expression in the developing otic placode and report the isolation of a novel core en

142 We have generated a fate map of the otic placode and show that precursors for vestibular and

143 demonstrate that both the enlargement of the otic placode and the expansion of the Wnt8a expression d

144 by the expression of Cre recombinase in the otic placode at E8.5.

145 Pax2(+) ectoderm gives rise not only to the otic placode but also to the surrounding cranial epiderm

146 e that the position of precursors within the otic placode confers identity to sensory organs and to t

147 Thus, different regions of the otic placode correspond to particular sense organs and t

148 Precursors from the anterior-lateral otic placode delaminate earlier than those from its medi

149 and Wnt pathways reveal that some aspects of otic placode development - such as Pax8 expression and t

150 esting that the regional organisation of the otic placode dictates positional cues to otic neurons.

151 ax8 and sox3 and support a model whereby the otic placode forms first and induces epibranchial placod

152 Amongst posterior placodes, the otic placode forms the inner ear whereas nearby epibranc

153 ression is unaffected in mutants in which no otic placode forms, where dlx3b and dlx4b are knocked do

154 y has been shown to regulate the size of the otic placode from which the cochlea will arise; however,

155 The otic placode generates the auditory and vestibular sense

156 The anterior-lateral portion of the otic placode generates vestibular neurons, whereas the p

157 Multipotent progenitor cells in the otic placode give rise to the specialized cell types of

158 that Wnt signaling specifies the size of the otic placode in two ways, by directly upregulating a sub

159 in-derived Wnt and Fgf signals specifies the otic placode in Xenopus, and promotes its morphogenesis

160 e incorporate into the otic epithelium after otic placode induction has occurred.

161 ompletely separable from its earlier role in otic placode induction.

162 actor spalt4 is a key early-response gene in otic placode induction.

163 as the role of dlx3b/4b function in PPR and otic placode induction.

164 During embryogenesis, the otic placode invaginates into the head to form the otic

165 trial primordium invagination are similar to otic placode invagination, but a placode-derived vesicle

166 os (Spry1(-)/(-); Spry2(-)/(-) embryos), the otic placode is increased in size.

167 We demonstrate that the otic placode is larger due to the recruitment of cells,

168 The enlargement of the otic placode observed in Spry1(-)/(-); Spry2(-)/(-) embr

169 ure epidermal cells, and with geniculate and otic placode precursors.

170 Conversely, loss of Spalt4 function in the otic placode results in abnormal otic vesicle developmen

171 human posterior cranial placodes such as the otic placode that gives rise to the inner ear do not exi

172 of the pre-otic field and restriction of the otic placode to ectoderm adjacent to the hindbrain.

173 sterior otic identity between the 10 somite (otic placode) and 20 somite (early otic vesicle) stages.

174 The otic placode, a specialized region of ectoderm, gives ri

175 n vertebrates, the inner ear arises from the otic placode, a thickened swathe of ectoderm that invagi

176 The vertebrate inner ear arises from the otic placode, a transient thickening of ectodermal epith

177 ble for the onset of Sox10 expression in the otic placode, as opposed to Myb plus Sox9 and Ets1 for n

178 Induction of the otic placode, the rudiment of the inner ear, is believed

179 It originates from the otic placode, which invaginates, forming the otic vesicl

180 involved in the initial specification of the otic placode.

181 required for the formation of the posterior otic placode.

182 yet it arises from a simple epithelium, the otic placode.

183 ontrols the onset of Sox10 expression in the otic placode.

184 enitor cell population for the inner ear, or otic placode.

185 ecialized region of head ectoderm termed the otic placode.

186 thickened patch of head ectoderm called the otic placode.

187 havior when WNT responses are blocked in the otic placode.

188 tch1 leads to a reduction in the size of the otic placode.

189 hought to share homology with the vertebrate otic placode.

190 streams and recruit sensory neurons from the otic placode; these ectopic neurons then extend axons be

191 equentially into non-neural, preplacodal and otic-placode-like epithelia.

192 prosensory cells emerge from the presumptive otic placodes and give rise to hair cells bearing stereo

193 acodes are not entirely resolved, vertebrate otic placodes and tunicate atrial siphon primordia are t

194 Olfactory and otic placodes, in combination with migratory neural cres

195 brain neurons, ttll4 in muscle, and ttll7 in otic placodes.

196 hich other local factors enhance or restrict otic potential.

197 t that Fgf and Hedgehog act on a symmetrical otic pre-pattern to specify anterior and posterior otic

198 ibranchial placode precursors lie lateral to otic precursors within a single Pax2a/8-positive domain;

199 ll trajectory analysis further revealed that otic progenitor cell types are induced in monolayer cult

200 The resulting otic progenitor cells were subjected to varying differen

201 forming positive feedback loops to stabilise otic progenitor identity.

202 We obtained two types of otic progenitors able to differentiate in vitro into hai

203 the selection process that determines which otic progenitors activate NEUROG1 and adopt a neuroblast

204 ng development, a select population of early otic progenitors express NEUROG1, delaminate from the ot

205 In the absence of Pax2, otic progenitors not only lose otic marker expression, b

206 t progenitors originate from Eya1-expressing otic progenitors.

207 This includes: 1) the prosensory otic region of high proliferation, neuroblast delaminati

208 f Gli3R required for the development of this otic region.

209 rimposed over both prosensory and nonsensory otic regions.

210 clarify the roles of foxi1 and pax2/8 in the otic response.

211 During development, otic sensory progenitors give rise to hair cells and sup

212 nct mechanisms: regulating the expression of otic specific genes and stimulating the proliferation of

213 ng-pathway-associated transcripts, and novel otic-specific genes.

214 s both necessary and sufficient for anterior otic specification during a similar period, a function t

215 se cells, termed "Conditionally Reprogrammed Otic Stem Cells" (CR-OSC), are able to bypass the senesc

216 genic line, results in the loss of posterior otic structures and a duplication of anterior domains.

217 itor SU5402, results in the loss of anterior otic structures and a mirror image duplication of poster

218 ased throughout the embryo, and dorsolateral otic structures are lost or reduced.

219 f Hh signalling activity causes ventromedial otic territories to expand at the expense of dorsolatera

220 on-specifying genes partially overlap in the otic territory, suggesting that mutual interactions amon

221 describe an open tubular ion chromatograph (OTIC) that uses anion exchange latex coated 5 mum radius

222 ncies regarding the ability of Fgf to induce otic tissue in ectopic locations, raising questions abou

223 measured the biomechanical properties of the otic tissues and modeled the acoustic propagation.

224 Otic tissues of mouse embryos carrying NCC lineage repor

225 Our results not only characterize the otic transcriptome in unprecedented detail, but also ide

226 n of canal projections and downregulation of otic versican expression in a hypomorphic lau allele can

227 lacode invaginates into the head to form the otic vesicle (OV), the primordium of the inner ear and C

228 r in cells that eventually contribute to the otic vesicle and epibranchial placodes.

229 on as brain, olfactory bulb, branchial arch, otic vesicle and fin enhancers, recapitulating dlx5a/6a

230 tracellular matrix production, push into the otic vesicle and fuse to form pillars.

231 to focus inductive WNT signals on the dorsal otic vesicle and highlighting a new example of cross-tal

232 yos had reduced numbers of hair cells in the otic vesicle and lateral line neuromasts with impaired s

233 , decreased sensory hair cell numbers in the otic vesicle and neuromasts, and abnormal sensory respon

234 so results in shorter tethering cilia in the otic vesicle and shorter motile cilia in the pronephric

235 originate as neuroblasts in the floor of the otic vesicle and subsequently delaminate and migrate tow

236 medial wall, but most cilia (92-98%) in the otic vesicle are immotile.

237 on of some cells from the medial wall of the otic vesicle but with a low incidence, suggesting the ac

238 Therefore, the otic vesicle case exemplifies a generic morphogenetic pr

239 During the developmental stages of otic vesicle closure and beginning morphogenesis, the fo

240 lacodes also downregulates Pax2 and disrupts otic vesicle closure, suggesting that Pax3 is sufficient

241 motile tether cilia at opposite poles of the otic vesicle create fluid vortices that attract otolith

242 own that the same Fgf signaling required for otic vesicle development is required for the development

243 tion in the otic placode results in abnormal otic vesicle development.

244 on-neural ectoderm, preplacodal ectoderm and otic vesicle epithelia.

245 Sox10 expression, it is necessary for later otic vesicle formation.

246 se filters, 12 of which are expressed in the otic vesicle in domains that overlap with Dlx5.

247 le ears (lte) mutant shows a collapse of the otic vesicle in the larva, apparently owing to a loss of

248 Injection of wild-type S. iniae into the otic vesicle induced a lethal infection by 24 h postinfe

249 l tuning during inner ear development as the otic vesicle initiates morphogenesis and prosensory cell

250 Patterning of the otic vesicle is apparently normal.

251 ehog (Shh), dorsoventral polarity within the otic vesicle is disrupted.

252 ticles, initially distributed throughout the otic vesicle lumen, become tethered to the tips of hair

253 ner ear epithelia during different stages of otic vesicle morphogenesis.

254 derived vesicle is never observed as for the otic vesicle of vertebrates.

255 of hair cell kinocilia (tether cilia) at the otic vesicle poles, forming two otoliths.

256 s, groups of motile cilia are present at the otic vesicle poles, surrounding the immotile tether cili

257 s still capable of tethering otoliths at the otic vesicle poles.

258 und that overexpression of Ntn1 in the chick otic vesicle prevented canal fusion by inhibiting apopto

259 f3a is dispensable for basal body docking in otic vesicle sensory epithelia and, surprisingly, short

260 imal when activated during placodal or early otic vesicle stages but declined rapidly thereafter.

261 0 somite (otic placode) and 20 somite (early otic vesicle) stages.

262 regulates expression of hmx2 and hmx3 in the otic vesicle, and conversely, hmx2 and hmx3 maintain the

263 arious organs, including the brain, eye, and otic vesicle, and these result in mortality within 7 day

264 homozygous embryos displayed defects in the otic vesicle, as previously reported in studies with mor

265 he vestibulo-ocular reflex consisting of the otic vesicle, cranial nerve VIII and vestibular ganglia.

266 l functions, including the jaw/snout region, otic vesicle, eye, and brain.

267 e expression patterns in the branchial arch, otic vesicle, forebrain and/or limb at embryonic day 11.

268 including the liver, heart, skeletal muscle, otic vesicle, forebrain, lateral line, and ganglions, mo

269 pment of the urogenital system, neural tube, otic vesicle, optic cup and optic tract.

270 to an increase in Wnt responsiveness in the otic vesicle, resulting in the ectopic expression of Tbx

271 of dorsolateral cell fates in the zebrafish otic vesicle, revealing distinct similarities between th

272 sculpted from pouches that protrude from the otic vesicle, the embryonic anlage of the inner ear.

273 ession of the same chicken Ntn1 in the mouse otic vesicle, where apoptosis is less prominent, resulte

274 lls types that produce it, specifically, the otic vesicle-derived progenitors that give rise to neuro

275 ween hindbrain-expressed Hoxa1 and Mafb, and otic vesicle-expressed Gbx2, in the genetic cascade init

276 more than half of these recombinants formed otic vesicle-like structures.

277 ed sensory development in all regions of the otic vesicle.

278 dorsal or lateral non-sensory regions of the otic vesicle.

279 grow out of a simple ball of epithelium, the otic vesicle.

280 to hindbrain rhombomeres (r) 5-6 to form the otic vesicle.

281 al and sensory progenitor pools in the whole otic vesicle.

282 on of Neurogenin1 (Ngn1) in the floor of the otic vesicle.

283 regulates delamination of neuroblasts in the otic vesicle.

284 the of ectoderm that invaginates to form the otic vesicle.

285 ia, all of which are found in the endogenous otic vesicle.

286 otic placode, which invaginates, forming the otic vesicle; the latter gives rise to neurosensory and

287 FGF, and WNT signaling to generate multiple otic-vesicle-like structures from a single stem-cell agg

288 Mutants developed enlarged otic vesicles and various defects of otoconia developmen

289 8 with Fgf8 potentiates formation of ectopic otic vesicles expressing a full range of otic markers.

290 expression profiling wild-type and Dlx5 null otic vesicles from embryonic stages E10 and E10.5.

291 ressed, sp8 was sufficient to induce ectopic otic vesicles possessing sensory hair cells, neurofilame

292 een 10 and 20 somites results in symmetrical otic vesicles with neither anterior nor posterior identi

293 s in the molecular patterning of Fgf3 mutant otic vesicles, and comparisons with other mutations affe

294 roof plate, epidermal multi-ciliated cells, otic vesicles, and kidneys.

295 is, such as uncompartmentalized and enlarged otic vesicles, epithelial dilation with abnormal sensory

296 RA signaling results in enlarged or reduced otic vesicles, respectively.

297 nts by morpholino injection results in small otic vesicles, similar to RA depletion in wild type.

298 ects left-right asymmetry of the embryo; the otic vesicles, which give rise to the inner ear; and the

299 nesis in the developing pronephric ducts and otic vesicles.

300 easibility of both isocratic and gradient SC-OTIC was demonstrated.