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

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

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

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

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

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

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

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

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

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

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

16 ithin the middle ear at the round window and otic capsule, induced precise shifts in the maximal vibr

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

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

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

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

21 er cells promote neurog1 expression in other otic cells.

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

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

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

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

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

27 Pan-otic CRE drivers enable gene regulation throughout the o

28 provides a useful complement to existing pan-otic CRE drivers, particularly for postnatal analyses.

29 Furthermore, extant pan-otic CREs recombine in auditory and vestibular brain nuc

30 t to analogous mice generated with other pan-otic CREs, these were viable.

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 fically cleared or down-regulated for proper otic development.

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

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

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

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

48 A single intra-otic dose of ASO corrects harmonin RNA splicing, restore

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

50 pitulates Pax2 expression in the presumptive otic ectoderm.

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

52 s or gain of SOX2 function led to changes in otic epithelial volume and progenitor proliferation, imp

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

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

55 ce, and observed CRE activity throughout the otic epithelium and neurons, with little activity eviden

56 resulting expression patterns in either the otic epithelium or its surrounding mesenchyme suggest th

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

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

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

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

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

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

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

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

65 and neurons overlap within the posteromedial otic epithelium.

66 of prosensory markers throughout the entire otic epithelium.

67 itory cells are regionally segregated in the otic epithelium.

68 lowing ectopic expression in chick embryonic otic epithelium.

69 Otic expression of extracellular matrix components is hi

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

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

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

73 and Foxd3 and inhibits otocyst formation and otic expression of Sox10 and Eya1.

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

75 Specification towards otic fate requires diverse signals and transcriptional i

76 which cooperate synergistically to establish otic fate.

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

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

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

80 ghlight the hierarchical organisation of the otic gene network.

81 However, intersection of extra-otic gene-of-interest expression with the CRE lineage ca

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

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

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

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

86 ecessary and sufficient to specify posterior otic identity.

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

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

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 e well-described elements of the response to otic injury and the otoprotective potential of JNK inhib

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

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

96 Otic lichen planus can lead to persistent hearing loss a

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

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

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

100 ells in vitro into functional hair cells and otic-like neurons.

101 Otic lineage cells differentiated from induced pluripote

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

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

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

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

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

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

108 asynchronous occurrences of preplacodal and otic marker genes.

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

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

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

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

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

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

115 1, which is required for Fgf to expand other otic markers.

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

117 Overall, these data suggest that otic mesenchyme cells may play a role in maintaining SGN

118 al ganglion neurons (SGNs) are surrounded by otic mesenchyme cells, which express the transcription f

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

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

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

122 demonstrates a novel role for SOX2 in early otic morphological development, and provides insights in

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 The resident identified otic pathology in 5% in baseline sequences and 20% using

135 nd 82.5% of extraotic pathology and 17.5% of otic pathology, highlighting the neurinoma of the VIII p

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

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

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

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

140 h is predominantly required for dorsoventral otic patterning.

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

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

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

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

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

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

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

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

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

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

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

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

153 The otic placode generates the auditory and vestibular sense

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

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

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

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

158 development, acting at multiple stages from otic placode induction to cellular differentiation in th

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

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

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

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

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

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

165 rivers enable gene regulation throughout the otic placode lineage, comprising the inner ear epitheliu

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

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

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

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

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

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

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

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

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

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

176 We have previously identified Slc26a9 as an otic placode-specific target of the FGFR2b ligands FGF3

177 involved in the initial specification of the otic placode.

178 required for the formation of the posterior otic placode.

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

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

181 ecialized region of head ectoderm termed the otic placode.

182 thickened patch of head ectoderm called the otic placode.

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

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

185 elopment from the formation of the embryonic otic placode.

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

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

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

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

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

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

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

193 hich other local factors enhance or restrict otic potential.

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

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

196 Selection of otic preparations to treat self-limited conditions with

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

198 The resulting otic progenitor cells were subjected to varying differen

199 forming positive feedback loops to stabilise otic progenitor identity.

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

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

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

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

204 t progenitors originate from Eya1-expressing otic progenitors.

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

206 rimposed over both prosensory and nonsensory otic regions.

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

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

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

210 We show here that Slc26a9 is otic specific through E10.5, but is not required for hea

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

212 Otic-specific knockout of bone morphogenetic protein 2 (

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

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

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

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

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

218 ics for neurosyphilis (as well as ocular and otic syphilis) are needed.

219 well as neurosyphilis, ocular syphilis, and otic syphilis).

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

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

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

223 g6 also results in defects in the inner ear: otic tissue fails to down-regulate versican gene express

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

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

226 Otic tissues of mouse embryos carrying NCC lineage repor

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

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

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

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

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

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

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

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

235 development of hair cells and neurons in the otic vesicle and other neurons in the CNS/PNS.

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

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

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

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

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

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

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

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

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

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

246 ne protected the hair cells in the zebrafish otic vesicle from cisplatin-induced damage and preserved

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

248 lea develops from a ventral outgrowth of the otic vesicle in response to Shh signaling.

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

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

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

252 Patterning of the otic vesicle is apparently normal.

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

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

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

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

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

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

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

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

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

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

263 t specific to all sensory regions until late otic vesicle stages.

264 op between pressure and transport allows the otic vesicle to change growth rate to control natural or

265 0 somite (otic placode) and 20 somite (early otic vesicle) stages.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

281 tress in the epithelium and expansion of the otic vesicle.

282 ession categories in the ventral half of the otic vesicle.

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

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

285 regulates delamination of neuroblasts in the otic vesicle.

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

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

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

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

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

291 8 with Fgf8 potentiates formation of ectopic otic vesicles expressing a full range of otic markers.

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

293 A comparative transcriptome analysis of otic vesicles from mouse mutants exhibiting loss (Smo(ec

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

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

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

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

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.