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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 cific genes were characteristic of different rhombomeres.
5 quire higher levels of RA than more anterior rhombomeres.
6 ior axis into a series of seven segments, or rhombomeres.
7 d neuroanatomically distinct segments called rhombomeres.
8 of well-defined neuroepithelial segments or rhombomeres.
9 sensory relay interneurons within individual rhombomeres.
10 dal hindbrain domain (r4-r7) into individual rhombomeres.
11 rt to confer the unique identity to multiple rhombomeres.
12 it promotes the specification of individual rhombomeres.
13 in hindbrain size and the loss of posterior rhombomeres.
14 regating populations of cells from different rhombomeres.
15 g that DBHR is regulated autonomously within rhombomeres.
16 ndbrain into lineage-restricted units called rhombomeres.
17 gulate the aberrant size of the misspecified rhombomeres.
18 xiting streams adjacent to the even-numbered rhombomeres.
19 divided into a series of compartments called rhombomeres.
20 ebrate embryonic hindbrain is segmented into rhombomeres.
21 ells emerged along the dorsal midline of all rhombomeres.
22 finity independently within their respective rhombomeres.
23 sharpen transition regions between different 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
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
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
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
40 we mapped the chick PrV nucleus position to rhombomere 1, confirming previous studies and in contras
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
52 results in an exclusion of those cells from rhombomeres 1 and 2, and in a simultaneous clustering al
55 n of ectopic somatic motoneurones in ventral rhombomeres 1-4, and was accompanied by the repression o
56 ebellum (diencephalic prosomere 1 through to rhombomere 11) play central roles in the processing of s
57 role in regulating the regional identity of rhombomere 2 (r2) and is the only Hox gene expressed in
58 Serotonergic neurons derived from former rhombomere 2 drive 90% of all hindbrain events at E11.5.
66 l funiculus, while the other originated from rhombomeres 2-5 and extended in the lateral funiculus.
67 treams of cranial NCCs migrating adjacent to rhombomeres 2-7 and that Fbln1-deficient embryos display
68 by a dramatic cell-fate misspecification in rhombomeres 2-7, which results in the production of supe
73 at by removing Otx2 function, development of rhombomere 3 is rescued in Gbx2(-/-) embryos, showing th
74 uncovered new domains of Hoxa1 expression in rhombomere 3, the otic epithelium, and cardiac precursor
75 n tissue microdissected from the prospective rhombomere 3-5 region of Hoxa1 null and wild type embryo
76 loss of premigratory neural crest cells from rhombomeres 3 and 5 (r3, r5) through programmed cell dea
77 pressed in the premigratory neural crest, in rhombomeres 3 and 5, and in the neural crest-derived mes
78 Nnat expression is first detected at E8.5 in rhombomeres 3 and 5, and subsequently, expression is wid
82 The activity of the paired Mauthner cells in rhombomere 4 (r4) has been shown to be critical for gene
83 o investigate chick NCC behaviors within the rhombomere 4 (r4) migratory stream by combining photoact
84 e invasion of cranial NCCs, specifically the rhombomere 4 (r4) migratory stream into branchial arch 2
85 usly to regulate FBM neuron migration out of rhombomere 4 (r4), but the cell-type within which it act
95 ced the formation of somatic motoneurones in rhombomere 4 only, and Hox genes normally expressed more
96 domain of fgf3 expression expands to include rhombomere 4 through rhombomere X (an aberrant segment t
98 ene expression at all axial levels except in rhombomere 4 was also reduced, suggesting an interferenc
99 of the sixth somite acquires the identity of rhombomere 4 when retinoic acid signalling is blocked.
100 lospinal neurons and posterior expansions of rhombomere 4, as well as defects in branchiomotor neuron
102 t background we demonstrate that presumptive rhombomere 4, the major site of origin of the second pha
107 haryngeal (nIX) motor neurons are induced in rhombomeres 4 and 6, respectively, and migrate tangentia
113 and NL are found in distinct regions within rhombomere 5, with NM precursors in medial regions and N
114 g-depleted embryos, suggesting a signal from rhombomere 5-6 may also be required for otic fate mainte
116 is specifically and transiently expressed in rhombomeres 5 and 6 (r5/r6), and Egr4 knockdown causes a
118 (val), which blocks early differentiation of rhombomeres 5 and 6 in the hindbrain, does not delay oti
119 uct formation indicating that signaling from rhombomeres 5 and 6 is important for cochlear duct patte
121 urgically generated chicken embryos in which rhombomeres 5 and 6 were similarly shifted relative to t
123 ical model, oculomotor circuits in hindbrain rhombomeres 5-6 develop and function independently of ho
124 de that the high expression of hox3 genes in rhombomeres 5-6 serves to prevent aberrant neuronal iden
126 which have disruptions in the development of rhombomeres 5-7 and in the third arch neural crest, and
129 n being detected in the premigratory NCCs in rhombomere 6 (r6), migrating NCCs, ventricular cardiomyo
130 bomere 5 affects cochlear duct growth, while rhombomere 6 removal affects cochlear growth and morphog
132 n patterns were identified; one derived from rhombomeres 6-7 that elongated in the dorsal funiculus,
133 l crest (arising from the level of hindbrain rhombomeres 6-8) contributes to the septation of the car
135 of lateral-directed NC cells, led by NC from rhombomere 7 (r7), move as a distinct subpopulation.
137 reticulospinal dINs in the caudal hindbrain (rhombomeres 7-8) fire significantly earlier on each swim
138 hombomeric boundary between rhombomere 7 and rhombomere 8 and between the most caudal rhombomere and
139 ong the anterior-posterior axis of hindbrain rhombomere 8 determines expression of hox5 genes, which
140 are together required for the development of rhombomeres adjacent to r4, particularly r5 and r6.
141 In contrast, removal of individual hindbrain rhombomeres adjacent to the developing ear preferentiall
142 st the hypothesis that a caudal shift of the rhombomeres affects inner ear development, we surgically
143 Following heterotopic transplantation of rhombomeres along the rostrocaudal axis at various devel
144 wn that cells at the boundaries of zebrafish rhombomeres also differ from non-boundary cells in their
146 and rhombomere 8 and between the most caudal rhombomere and the spinal cord was not nearly as clear a
147 construction demonstrates cell shapes within rhombomeres and at rhombomere boundaries are abnormal in
149 omere boundaries, subsequent openings within rhombomeres and eventual coalescence of openings into th
151 ntagonist, is expressed in the even-numbered rhombomeres and that over-expression of cSfrp2 inhibits
152 nds, ephrins, are expressed in complementary rhombomeres and, by analogy with their roles in axon pat
153 xing of neural crest cells between adjoining rhombomeres, and the diversity in cell migration behavio
155 However, later antagonist treatments after rhombomeres are established still disrupt branchiomotor
160 xing of neural crest cells between adjoining rhombomeres as cells emerged from the dorsal midline; th
162 Increasing noise disrupts sharpening of rhombomere boundaries and proper patterning of the hindb
163 trates cell shapes within rhombomeres and at rhombomere boundaries are abnormal in mypt1 mutants.
164 ith antisense morpholinos (MO) and find that rhombomere boundaries are disrupted in EphA4MO embryos,
165 effectors that bring about the formation of rhombomere boundaries are only just being characterized.
166 Transplantation studies have suggested that rhombomere boundaries form by the local sorting out of c
170 onist shows that successively more posterior rhombomere boundaries require progressively higher conce
171 cond and unique role in the morphogenesis of rhombomere boundaries, indicating that it controls multi
172 with initial separation along the midline at rhombomere boundaries, subsequent openings within rhombo
179 ntin remains localized in radial glia at the rhombomere boundary regions, whereas expression of glial
185 operties of odd- and even-numbered segments (rhombomeres), but an adhesion molecule with alternating
186 is an early embryonic signal that specifies rhombomeres, but its roles in neuronal differentiation w
187 ges shows that the neurons of IF5 arise from rhombomeres caudal to rhombomere 4, most likely from rho
188 buted these defects to a caudal shift of the rhombomeres caused by the shortened body axis and the ki
189 ducibly penetrate into the hindbrain via the rhombomere centers, where differentiated neurons reside,
190 r become confined to the ventricular zone at rhombomere centers, whereas the protein is exclusively e
191 Furthermore, the persistence of some normal rhombomere characteristics in Hox mutant embryos suggest
197 which is organized in a metameric series of rhombomere-derived (rd) territories, follows a rhombomer
198 lel with the EphA4-dependent adhesion within rhombomeres described here to drive the cell sorting tha
202 ur data demonstrate that, in contrast to the rhombomeres, differential adhesion does not seem to oper
203 ndbrain opening remains normal, mypt1 mutant rhombomeres do not undergo normal morphological progress
204 radial glia but subsequently define distinct rhombomere domains: vimentin remains localized in radial
205 rtebrate hindbrain leads to the formation of rhombomeres, each with a distinct anteroposterior identi
208 in hindbrain development is specification of rhombomere identities and that the aberrant development
209 e' is required for the development of unique rhombomere identities, including specification of neuron
210 Thus, in addition to its role in determining rhombomere identities, RA plays a more direct role in th
217 m contains contributions of cells from three rhombomeres in a pattern very similar to that observed i
218 hox function disrupts development of caudal rhombomeres in model organisms and causes brainstem defe
220 equired for anterior-posterior patterning of rhombomeres in the hindbrain, there are unique requireme
222 ocus on the formation of hindbrain segments (rhombomeres) in the developing zebrafish as an example,
224 other Hox proteins expressed at more rostral rhombomere interfaces can also regulate Eph/ephrins, ind
225 egated streams adjacent to the even-numbered rhombomeres into the branchial arches, and each stream c
226 and regionally specific structures from each rhombomere is achieved with the almost complete absence
228 egmentation of the vertebrate hindbrain into rhombomeres is a key step in the development of a comple
229 on of the vertebrate hindbrain into multiple rhombomeres is essential for proper formation of the cer
230 egmentation of the vertebrate hindbrain into rhombomeres is essential for the anterior-posterior patt
231 egmentation of the vertebrate hindbrain into rhombomeres is highly conserved, but how early hindbrain
232 ansient, genetically-defined segments called rhombomeres is required for normal respiratory developme
234 hat extent neural crest cells from adjoining rhombomeres mix along migration routes and within the br
235 that in the zebrafish hindbrain, cell shape, rhombomere morphogenesis and, unexpectedly, brain ventri
238 c movements of precursor cells establish the rhombomeres of the hindbrain, the external germinal laye
241 ttern that corresponds with the segments, or rhombomeres, of the developing hindbrain and have identi
242 well-known EphA4-dependent repulsion between rhombomeres operates in parallel with the EphA4-dependen
243 ffinity within rhombomeres serve to maintain rhombomere organization during the potentially disruptiv
246 n the hindbrain, both genes are expressed in rhombomere (r) 2, but only Hoxa2(b) is expressed in r3,
247 in the cytoplasm leads to extensive loss of rhombomere (r) 3- and r4-specific gene expression, as we
249 rostral expression limit at the presumptive rhombomere (r) 3/r4 boundary during gastrula stages, and
250 chiomotor (FBM) neurones are born in ventral rhombomere (r) 4 and migrate through r5 to dorsal r6 whe
252 angential migration from their birthplace in rhombomere (r) 4 to their final destination in r6/r7.
255 nds from the posterior spinal cord up to the rhombomere (r) 4/5 boundary and both genes are upregulat
256 red cell autonomously for the development of rhombomere (r) 5 and r6 and for activation of Hox group
258 tory streams that emerge from the hindbrain, rhombomere (r) segments r1-r7, and the signals that coor
259 e neural tube that had never expressed Hoxb [rhombomeres (r) 1 and 2], strongly expressed Hoxb1 but n
261 w that distinct combinations of Hox genes in rhombomeres (r) 4 and 5 of the hindbrain are required fo
263 neuronal populations derived from hindbrain rhombomeres (r) 5 to 8, suggesting a late role of the ge
265 owed that neural crest cells emerge from all rhombomeres (r) and sort into distinct exiting streams a
266 tinoic acid, and specification of individual rhombomeres (r) follows a strict rostrocaudal sequence a
267 rate hindbrain is segmented into an array of rhombomeres (r), but it remains to be fully understood h
271 he hindbrain into the mesenchyme adjacent to rhombomeres (r)1 plus r2, r4 and r6 in three segregated
274 , a key segmentation factor expressed in odd rhombomeres (r3 and r5), can largely override Hox protei
275 (RENs) that arises in the fourth segment, or rhombomere (r4), of the hindbrain and a group of caudal
276 ommon olig2(+) neuroepithelial precursors in rhombomeres r5 and r6, but that all other motor neurons
278 ion of these factors and that more posterior rhombomeres require higher levels of RA than more anteri
279 g, we show that progressively more posterior rhombomeres require increasingly higher levels of RA sig
281 sulted in the homeotic transformation of the rhombomere, revealed by reorganization of motor axon pro
284 cdx4 overexpression in the hindbrain impairs rhombomere segmentation and patterning and induces the e
285 h Eph and Efn-dependent cell affinity within rhombomeres serve to maintain rhombomere organization du
287 strate a crucial role for FGF-mediated inter-rhombomere signaling in promoting early hindbrain patter
288 and their ligands, the ephrins, function in rhombomere-specific cell sorting and initiation of a str
289 ombomere-derived (rd) territories, follows a rhombomere-specific pattern, with extensive production o
291 ically and molecularly distinct segments, or rhombomeres, that correspond to Hox expression domains.
293 ntervein divisions of the wing and mammalian rhombomeres, the Nub and Tsh domains share some of the a
295 l stages, we have found that the capacity of rhombomeres to generate somatic motoneurones is labile a
296 a suggest that an early event in determining rhombomere topology is the specification of both morphol
297 ct border between the midbrain and the first rhombomere was not seen and the isthmic rhombomere could
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