ライフサイエンスコーパス: rhombomere

1 ecify distinct neuronal lineages within each rhombomere.

2 -like facial branchiomotoneurons within this rhombomere.

3 sed but not when midbrain contacts any other rhombomere.

4 quire higher levels of RA than more anterior rhombomeres.

5 ior axis into a series of seven segments, or rhombomeres.

6 d neuroanatomically distinct segments called rhombomeres.

7 in hindbrain size and the loss of posterior rhombomeres.

8 sensory relay interneurons within individual rhombomeres.

9 dal hindbrain domain (r4-r7) into individual rhombomeres.

10 rt to confer the unique identity to multiple rhombomeres.

11 it promotes the specification of individual rhombomeres.

12 ndbrain into lineage-restricted units called rhombomeres.

13 regating populations of cells from different rhombomeres.

14 g that DBHR is regulated autonomously within rhombomeres.

15 gulate the aberrant size of the misspecified rhombomeres.

16 xiting streams adjacent to the even-numbered rhombomeres.

17 divided into a series of compartments called rhombomeres.

18 ebrate embryonic hindbrain is segmented into rhombomeres.

19 ells emerged along the dorsal midline of all rhombomeres.

20 ts in sorting to boundaries in even-numbered rhombomeres.

21 sharpen transition regions between different rhombomeres.

22 finity independently within their respective rhombomeres.

23 of well-defined neuroepithelial segments or rhombomeres.

24 t to Gbx2 null mutants, mice lacking Gbx2 in rhombomere 1 (r1) after E9 (Gbx2-CKO) are viable and dev

25 V) patterning of the mesencephalon (mes) and rhombomere 1 (r1) is instrumental for the development of

26 ng the midbrain, and induces a cerebellum in rhombomere 1 (r1) is not clear.

27 res derived from the mesencephalon (mes) and rhombomere 1 (r1) modulate distinct motor and sensory mo

28 the induction of rostral 5-HT neurons within rhombomere 1 (r1), which project to the forebrain, but n

29 part of the anterior-most hindbrain segment, rhombomere 1 (r1), which undergoes a distinctive morphog

30 e presumptive mesencephalon into an extended rhombomere 1 (r1).

31 2 converts the rostral-caudal axis of dorsal rhombomere 1 into the medial-lateral axis of the wing-li

32 ecific grafting strategy we demonstrate that rhombomere 1 is able to express Hox genes but that both

33 The unique developmental fate of rhombomere 1 is reflected by it being the only hindbrain

34 In rhombomere 1 of the chick, early born cells give rise to

35 e demonstrate that secreted signals from the rhombomere 1 roof plate are both necessary and sufficien

36 mic organiser is generated when midbrain and rhombomere 1 tissue are juxtaposed but not when midbrain

37 use midbrain (mesencephalon) and cerebellum (rhombomere 1) by misexpressing sprouty2 (Spry2) from an

38 phalon (mes) and rostral metencephalon (met; rhombomere 1), respectively.

39 In rhombomere 1, Atoh1-positive cells give rise to both cer

40 we mapped the chick PrV nucleus position to rhombomere 1, confirming previous studies and in contras

41 nterior segment of the vertebrate hindbrain, rhombomere 1, gives rise to the entire cerebellum.

42 Early born cells, which migrate into ventral rhombomere 1, have a single long leading process that tu

43 By fate mapping the dorsoventral axis of rhombomere 1, we demonstrate that granule cell precursor

44 lip gives rise to multiple cell types within rhombomere 1.

45 also immediately posterior to it in anterior rhombomere 1.

46 hin the hindbrain in a manner appropriate to rhombomere 1.

47 ebellum at E6 maps to the caudal boundary of rhombomere 1.

48 t the isthmic tissue is largely derived from rhombomere 1.

49 the IP develops strictly within isthmus and rhombomere 1.

50 between vermis and roof plate development in rhombomere 1.

51 results in an exclusion of those cells from rhombomeres 1 and 2, and in a simultaneous clustering al

52 Strong FRMD7 expression was seen in rhombomeres 1 to 4, which give rise to the cerebellum an

53 ring gastrulation, and becomes restricted to rhombomeres 1-3 (r1-3) by embryonic day 8.5 (E8.5).

54 n of ectopic somatic motoneurones in ventral rhombomeres 1-4, and was accompanied by the repression o

55 role in regulating the regional identity of rhombomere 2 (r2) and is the only Hox gene expressed in

56 Serotonergic neurons derived from former rhombomere 2 drive 90% of all hindbrain events at E11.5.

57 ether to induce ectopic hoxb1a expression in rhombomere 2 of the hindbrain.

58 contrast to mouse PrV, which mainly maps to rhombomere 2-3.

59 lamprey that drives segmental expression in rhombomeres 2 and 4.

60 Development of rhombomeres 2 through 5 was investigated in wholemount p

61 When present, boundaries of rhombomeres 2 through 5 were distinct.

62 ifferential growth sculpts the morphology of rhombomeres 2 through 5.

63 ot nearly as clear as were the boundaries of rhombomeres 2 through 5.

64 l funiculus, while the other originated from rhombomeres 2-5 and extended in the lateral funiculus.

65 treams of cranial NCCs migrating adjacent to rhombomeres 2-7 and that Fbln1-deficient embryos display

66 by a dramatic cell-fate misspecification in rhombomeres 2-7, which results in the production of supe

67 e absence of cell mixing between neighboring rhombomeres [2, 3].

68 Neural crest cell-free zones lateral to rhombomere 3 (r3) and r5 resulted from neural crest cell

69 plays a permissive, not instructive, role in rhombomere 3 development.

70 ion of Lim1 lack head structures anterior to rhombomere 3 in the hindbrain.

71 at by removing Otx2 function, development of rhombomere 3 is rescued in Gbx2(-/-) embryos, showing th

72 uncovered new domains of Hoxa1 expression in rhombomere 3, the otic epithelium, and cardiac precursor

73 n tissue microdissected from the prospective rhombomere 3-5 region of Hoxa1 null and wild type embryo

74 loss of premigratory neural crest cells from rhombomeres 3 and 5 (r3, r5) through programmed cell dea

75 pressed in the premigratory neural crest, in rhombomeres 3 and 5, and in the neural crest-derived mes

76 Nnat expression is first detected at E8.5 in rhombomeres 3 and 5, and subsequently, expression is wid

77 ain patterning for the normal development of rhombomeres 3 and 5.

78 ically rotated the rostrocaudal positions of rhombomeres 3/4.

79 We show that rhombomere 4 (r4) functions as an early-differentiating

80 The activity of the paired Mauthner cells in rhombomere 4 (r4) has been shown to be critical for gene

81 o investigate chick NCC behaviors within the rhombomere 4 (r4) migratory stream by combining photoact

82 e invasion of cranial NCCs, specifically the rhombomere 4 (r4) migratory stream into branchial arch 2

83 usly to regulate FBM neuron migration out of rhombomere 4 (r4), but the cell-type within which it act

84 Hoxb1, which is expressed throughout rhombomere 4 (r4), has been shown to be required for the

85 striction of Hoxb1 expression to presumptive rhombomere 4 (r4).

86 red for segment boundary formation caudal to rhombomere 4 (r4).

87 progenitor cells along the entire DV axis of rhombomere 4 (r4).

88 equired for proper segmental organization of rhombomere 4 and the posterior hindbrain.

89 epiboly and are induced in the primordium of rhombomere 4 by 80% epibloy.

90 f the earliest hindbrain signaling-center in rhombomere 4 by regulating expression of fgf3.

91 rain boundary and in the hindbrain caudal to rhombomere 4 during segmentation.

92 y facial motor neurons do not migrate out of rhombomere 4 into more posterior segments.

93 ced the formation of somatic motoneurones in rhombomere 4 only, and Hox genes normally expressed more

94 domain of fgf3 expression expands to include rhombomere 4 through rhombomere X (an aberrant segment t

95 rons from their point of origin in hindbrain rhombomere 4 towards the posterior.

96 ene expression at all axial levels except in rhombomere 4 was also reduced, suggesting an interferenc

97 of the sixth somite acquires the identity of rhombomere 4 when retinoic acid signalling is blocked.

98 lospinal neurons and posterior expansions of rhombomere 4, as well as defects in branchiomotor neuron

99 rons of IF5 arise from rhombomeres caudal to rhombomere 4, most likely from rhombomeres 6-8.

100 t background we demonstrate that presumptive rhombomere 4, the major site of origin of the second pha

101 n fates, including differentiation of excess rhombomere 4-specific Mauthner neurons.

102 d influence the fate of cells originating in rhombomere 4.

103 to directly regulate ppp1r14al expression in rhombomere 4.

104 Examples include: the loss of both rhombomeres 4 and 5, the selective loss of the 2(nd) bra

105 haryngeal (nIX) motor neurons are induced in rhombomeres 4 and 6, respectively, and migrate tangentia

106 osis in areas populated by NCCs derived from rhombomeres 4, 6 and 7.

107 Removal of rhombomere 5 affects cochlear duct growth, while rhombom

108 d that activity in a small hindbrain area in rhombomere 5 was necessary for saccades to occur.

109 We show that rhombomere 5 wnt8b expression is absent in both RA-signa

110 EphA4 is expressed in rhombomere 5, which contains progenitors for both NM and

111 and NL are found in distinct regions within rhombomere 5, with NM precursors in medial regions and N

112 g-depleted embryos, suggesting a signal from rhombomere 5-6 may also be required for otic fate mainte

113 nuclear factor 1 (vhnf1) in specification of rhombomeres 5 and 6 (r5+r6).

114 is specifically and transiently expressed in rhombomeres 5 and 6 (r5/r6), and Egr4 knockdown causes a

115 Rotating rhombomeres 5 and 6 along the anteroposterior axis also

116 (val), which blocks early differentiation of rhombomeres 5 and 6 in the hindbrain, does not delay oti

117 uct formation indicating that signaling from rhombomeres 5 and 6 is important for cochlear duct patte

118 Signaling from rhombomeres 5 and 6 of the hindbrain is thought to be im

119 urgically generated chicken embryos in which rhombomeres 5 and 6 were similarly shifted relative to t

120 X (an aberrant segment that forms in lieu of rhombomeres 5 and 6).

121 ical model, oculomotor circuits in hindbrain rhombomeres 5-6 develop and function independently of ho

122 de that the high expression of hox3 genes in rhombomeres 5-6 serves to prevent aberrant neuronal iden

123 convergence to their final position next to rhombomeres 5-6.

124 which have disruptions in the development of rhombomeres 5-7 and in the third arch neural crest, and

125 population of central vestibular neurons in rhombomeres 5-7 of larval zebrafish.

126 are confined to the caudal hindbrain within rhombomeres 5-8.

127 n being detected in the premigratory NCCs in rhombomere 6 (r6), migrating NCCs, ventricular cardiomyo

128 bomere 5 affects cochlear duct growth, while rhombomere 6 removal affects cochlear growth and morphog

129 g cranial nerves IX and X, which derive from rhombomeres 6 and 7.

130 n patterns were identified; one derived from rhombomeres 6-7 that elongated in the dorsal funiculus,

131 l crest (arising from the level of hindbrain rhombomeres 6-8) contributes to the septation of the car

132 res caudal to rhombomere 4, most likely from rhombomeres 6-8.

133 of lateral-directed NC cells, led by NC from rhombomere 7 (r7), move as a distinct subpopulation.

134 The interrhombomeric boundary between rhombomere 7 and rhombomere 8 and between the most cauda

135 reticulospinal dINs in the caudal hindbrain (rhombomeres 7-8) fire significantly earlier on each swim

136 hombomeric boundary between rhombomere 7 and rhombomere 8 and between the most caudal rhombomere and

137 ong the anterior-posterior axis of hindbrain rhombomere 8 determines expression of hox5 genes, which

138 are together required for the development of rhombomeres adjacent to r4, particularly r5 and r6.

139 In contrast, removal of individual hindbrain rhombomeres adjacent to the developing ear preferentiall

140 st the hypothesis that a caudal shift of the rhombomeres affects inner ear development, we surgically

141 Following heterotopic transplantation of rhombomeres along the rostrocaudal axis at various devel

142 wn that cells at the boundaries of zebrafish rhombomeres also differ from non-boundary cells in their

143 a mismatch in Hox coding between a specific rhombomere and its corresponding branchial arch.

144 and rhombomere 8 and between the most caudal rhombomere and the spinal cord was not nearly as clear a

145 construction demonstrates cell shapes within rhombomeres and at rhombomere boundaries are abnormal in

146 allow Hoxa2 to be regulated independently in rhombomeres and cranial neural crest cells.

147 omere boundaries, subsequent openings within rhombomeres and eventual coalescence of openings into th

148 y and anteroposterior character of hindbrain rhombomeres and neural crest-derived structures.

149 ntagonist, is expressed in the even-numbered rhombomeres and that over-expression of cSfrp2 inhibits

150 nds, ephrins, are expressed in complementary rhombomeres and, by analogy with their roles in axon pat

151 xing of neural crest cells between adjoining rhombomeres, and the diversity in cell migration behavio

152 ures that define boundaries between adjacent rhombomeres are as yet unclear.

153 However, later antagonist treatments after rhombomeres are established still disrupt branchiomotor

154 erentiated neurons reside, and that specific rhombomeres are invariably vascularized first.

155 mbomere boundaries form sequentially until 8 rhombomeres are present at stage 8.

156 Rhombomeres are segmental units of the developing verteb

157 While rhombomeres are visible in all vertebrate embryos, gener

158 xing of neural crest cells between adjoining rhombomeres as cells emerged from the dorsal midline; th

159 From stage 11 onwards, rhombomere borders fade.

160 Increasing noise disrupts sharpening of rhombomere boundaries and proper patterning of the hindb

161 trates cell shapes within rhombomeres and at rhombomere boundaries are abnormal in mypt1 mutants.

162 ith antisense morpholinos (MO) and find that rhombomere boundaries are disrupted in EphA4MO embryos,

163 effectors that bring about the formation of rhombomere boundaries are only just being characterized.

164 Transplantation studies have suggested that rhombomere boundaries form by the local sorting out of c

165 Rhombomere boundaries form sequentially until 8 rhombome

166 Specification of future rhombomere boundaries has a retinoic acid dependency bet

167 enesis becomes confined to zones adjacent to rhombomere boundaries in the zebrafish hindbrain.

168 onist shows that successively more posterior rhombomere boundaries require progressively higher conce

169 cond and unique role in the morphogenesis of rhombomere boundaries, indicating that it controls multi

170 with initial separation along the midline at rhombomere boundaries, subsequent openings within rhombo

171 orting and plasticity -- to the formation of rhombomere boundaries.

172 um, and myosin II and actin concentration at rhombomere boundaries.

173 or cell segregation, and for the most caudal rhombomere boundary (r6/r7).

174 ecific gene expression, as well as defective rhombomere boundary formation in this region.

175 e ephrins, are candidates for functioning in rhombomere boundary formation.

176 nts in the early hindbrain, are required for rhombomere boundary formation.

177 ntin remains localized in radial glia at the rhombomere boundary regions, whereas expression of glial

178 radial glial cell processes that occupy the rhombomere boundary regions.

179 Finally, we show that dorsal rhombomere boundary signaling centers depend on Zic1 and

180 of Hoxb1 expression at the presumptive r3/4 rhombomere boundary.

181 Although a model for rhombomere-boundary formation based on repulsive Eph-eph

182 ere to drive the cell sorting that underlies rhombomere-boundary formation.

183 operties of odd- and even-numbered segments (rhombomeres), but an adhesion molecule with alternating

184 is an early embryonic signal that specifies rhombomeres, but its roles in neuronal differentiation w

185 ges shows that the neurons of IF5 arise from rhombomeres caudal to rhombomere 4, most likely from rho

186 buted these defects to a caudal shift of the rhombomeres caused by the shortened body axis and the ki

187 ducibly penetrate into the hindbrain via the rhombomere centers, where differentiated neurons reside,

188 r become confined to the ventricular zone at rhombomere centers, whereas the protein is exclusively e

189 Furthermore, the persistence of some normal rhombomere characteristics in Hox mutant embryos suggest

190 Despite their ectopic position, both rhombomeres continued to express DBHR at the level appro

191 d proposed that preferential adhesion within rhombomeres contributes to boundary formation.

192 irst rhombomere was not seen and the isthmic rhombomere could not be identified.

193 and developing vasculature (Cyp26B1) and the rhombomeres (Cyp26C1).

194 In the hindbrain, rhombomeres demarcate nonoverlapping regions of the CNS

195 which is organized in a metameric series of rhombomere-derived (rd) territories, follows a rhombomer

196 lel with the EphA4-dependent adhesion within rhombomeres described here to drive the cell sorting tha

197 ighly conserved process but the mechanism of rhombomere determination is not well understood.

198 Rhombomere development in Alligator shares several featu

199 Rhombomere development was investigated in a reptile, Al

200 ur data demonstrate that, in contrast to the rhombomeres, differential adhesion does not seem to oper

201 ndbrain opening remains normal, mypt1 mutant rhombomeres do not undergo normal morphological progress

202 radial glia but subsequently define distinct rhombomere domains: vimentin remains localized in radial

203 Rhombomere formation and the development of other hindbr

204 in the caudal hindbrain and are required for rhombomere formation.

205 in hindbrain development is specification of rhombomere identities and that the aberrant development

206 e' is required for the development of unique rhombomere identities, including specification of neuron

207 Thus, in addition to its role in determining rhombomere identities, RA plays a more direct role in th

208 tially initiate progressively more posterior rhombomere identities.

209 inding transcription complexes which specify rhombomere identities.

210 stablishing the segmental plan and assigning rhombomere identity are now known.

211 lations may result, in part, from defects in rhombomere identity.

212 ons cannot be explained solely by changes in rhombomere identity.

213 In val(-) mutants, rX, a region one rhombomere in length and of mixed identity, lies between

214 The identification of rhombomeres in a multitude of vertebrates from a variety

215 m contains contributions of cells from three rhombomeres in a pattern very similar to that observed i

216 hox function disrupts development of caudal rhombomeres in model organisms and causes brainstem defe

217 that ensure distinction between the multiple rhombomeres in the developing hindbrain.

218 equired for anterior-posterior patterning of rhombomeres in the hindbrain, there are unique requireme

219 that EphA4 promotes cell adhesion within the rhombomeres in which it is expressed.

220 ocus on the formation of hindbrain segments (rhombomeres) in the developing zebrafish as an example,

221 se affects patterning of hindbrain segments (rhombomeres) in the zebrafish embryo.

222 other Hox proteins expressed at more rostral rhombomere interfaces can also regulate Eph/ephrins, ind

223 egated streams adjacent to the even-numbered rhombomeres into the branchial arches, and each stream c

224 and regionally specific structures from each rhombomere is achieved with the almost complete absence

225 The identity of each rhombomere is specified by the expression of conserved t

226 egmentation of the vertebrate hindbrain into rhombomeres is a key step in the development of a comple

227 on of the vertebrate hindbrain into multiple rhombomeres is essential for proper formation of the cer

228 egmentation of the vertebrate hindbrain into rhombomeres is essential for the anterior-posterior patt

229 egmentation of the vertebrate hindbrain into rhombomeres is highly conserved, but how early hindbrain

230 ansient, genetically-defined segments called rhombomeres is required for normal respiratory developme

231 Hence, vertebrate rhombomeres may derive from a cryptically segmented brai

232 hat extent neural crest cells from adjoining rhombomeres mix along migration routes and within the br

233 that in the zebrafish hindbrain, cell shape, rhombomere morphogenesis and, unexpectedly, brain ventri

234 Brain ventricle lumen expansion, rhombomere morphology and cell shape are rescued by inhi

235 NM and NL thus have partially overlapping rhombomeres of origin.

236 c movements of precursor cells establish the rhombomeres of the hindbrain, the external germinal laye

237 eloping vertebrates occurs between adjacent -rhombomeres of the hindbrain.

238 of the neural tube, including even-numbered rhombomeres of the hindbrain.

239 ttern that corresponds with the segments, or rhombomeres, of the developing hindbrain and have identi

240 well-known EphA4-dependent repulsion between rhombomeres operates in parallel with the EphA4-dependen

241 ffinity within rhombomeres serve to maintain rhombomere organization during the potentially disruptiv

242 Hindbrain rhombomere patterning and the initial generation of post

243 pletely or partially fused from the level of rhombomere (r) 2 towards the posterior.

244 n the hindbrain, both genes are expressed in rhombomere (r) 2, but only Hoxa2(b) is expressed in r3,

245 in the cytoplasm leads to extensive loss of rhombomere (r) 3- and r4-specific gene expression, as we

246 loss of hindbrain segmentation caudal to the rhombomere (r) 3/4 border in a subset of embryos.

247 rostral expression limit at the presumptive rhombomere (r) 3/r4 boundary during gastrula stages, and

248 chiomotor (FBM) neurones are born in ventral rhombomere (r) 4 and migrate through r5 to dorsal r6 whe

249 FBM neurons failed to migrate caudally from rhombomere (r) 4 into r6.

250 angential migration from their birthplace in rhombomere (r) 4 to their final destination in r6/r7.

251 evelopment, conferring identity to hindbrain rhombomere (r) 4.

252 anistic basis for the regulation of Hoxa2 in rhombomere (r) 4.

253 nds from the posterior spinal cord up to the rhombomere (r) 4/5 boundary and both genes are upregulat

254 red cell autonomously for the development of rhombomere (r) 5 and r6 and for activation of Hox group

255 s revealed some of their roles in specifying rhombomere (r) identity.

256 tory streams that emerge from the hindbrain, rhombomere (r) segments r1-r7, and the signals that coor

257 trigeminal ganglion axons always project to rhombomere (r)2, whilst facial/acoustic ganglia axons al

258 e neural tube that had never expressed Hoxb [rhombomeres (r) 1 and 2], strongly expressed Hoxb1 but n

259 In Gbx2 null homozygotes, rhombomeres (r) 1-3 fail to develop and the isthmic expr

260 w that distinct combinations of Hox genes in rhombomeres (r) 4 and 5 of the hindbrain are required fo

261 are expressed at high relative levels in the rhombomeres (r) 5 and 6, and 5, respectively.

262 neuronal populations derived from hindbrain rhombomeres (r) 5 to 8, suggesting a late role of the ge

263 lacode that invaginates lateral to hindbrain rhombomeres (r) 5-6 to form the otic vesicle.

264 owed that neural crest cells emerge from all rhombomeres (r) and sort into distinct exiting streams a

265 tinoic acid, and specification of individual rhombomeres (r) follows a strict rostrocaudal sequence a

266 rate hindbrain is segmented into an array of rhombomeres (r), but it remains to be fully understood h

267 at interfaces between neural segments called rhombomeres (r).

268 vided into serially homologous segments, the rhombomeres (r).

269 ain is transiently segmented into 7 distinct rhombomeres (r).

270 he hindbrain into the mesenchyme adjacent to rhombomeres (r)1 plus r2, r4 and r6 in three segregated

271 o three streams, with mesenchyme adjacent to rhombomeres (r)3 and r5 maintained NCC-free.

272 In these rhombomeres, r2 through r5, rostrocaudal caudal expansio

273 , a key segmentation factor expressed in odd rhombomeres (r3 and r5), can largely override Hox protei

274 ommon olig2(+) neuroepithelial precursors in rhombomeres r5 and r6, but that all other motor neurons

275 We found that NM arises from rhombomeres r5, r6, and r7, and NL arises mostly from r5

276 ion of these factors and that more posterior rhombomeres require higher levels of RA than more anteri

277 g, we show that progressively more posterior rhombomeres require increasingly higher levels of RA sig

278 Rhombomere-restricted misexpression of a single gene, Ho

279 sulted in the homeotic transformation of the rhombomere, revealed by reorganization of motor axon pro

280 ion originate from the same caudal hindbrain rhombomere (rh) 8-spinal compartment.

281 strate that not all aspects of an individual rhombomere's identity are regulated coordinately.

282 cdx4 overexpression in the hindbrain impairs rhombomere segmentation and patterning and induces the e

283 h Eph and Efn-dependent cell affinity within rhombomeres serve to maintain rhombomere organization du

284 All chicken embryos with shifted rhombomeres showed defects in cochlear duct formation in

285 strate a crucial role for FGF-mediated inter-rhombomere signaling in promoting early hindbrain patter

286 and their ligands, the ephrins, function in rhombomere-specific cell sorting and initiation of a str

287 ombomere-derived (rd) territories, follows a rhombomere-specific pattern, with extensive production o

288 We show that early zebrafish rhombomere-specification genes, including vhnf1 in r5-r6

289 ically and molecularly distinct segments, or rhombomeres, that correspond to Hox expression domains.

290 In this rhombomere, the labeling becomes striped during the time

291 ntervein divisions of the wing and mammalian rhombomeres, the Nub and Tsh domains share some of the a

292 Whereas the hindbrain subdivides into rhombomeres, the spinal cord remains unsegmented.

293 l stages, we have found that the capacity of rhombomeres to generate somatic motoneurones is labile a

294 a suggest that an early event in determining rhombomere topology is the specification of both morphol

295 ct border between the midbrain and the first rhombomere was not seen and the isthmic rhombomere could

296 rting of cells to boundaries in odd-numbered rhombomeres, whereas mosaic activation of ephrins result

297 s organized into a series of segments termed rhombomeres which represent lineage restricted compartme

298 ization of neural crest cells from adjoining rhombomeres within a single branchial arch support the n

299 through two phases, the misspecification of rhombomeres within the hindbrain, followed subsequently

300 sion expands to include rhombomere 4 through rhombomere X (an aberrant segment that forms in lieu of