ライフサイエンスコーパス: otocyst

1 he periotic mesenchyme surrounding the chick otocyst.

2 sensory-competent region in the rudimentary otocyst.

3 E2 and E3.5, neuroblasts delaminate from the otocyst.

4 a, seem to arise from a single region of the otocyst.

5 ecifically expressed in the developing mouse otocyst.

6 with dysgenesis of the pars inferior of the otocyst.

7 progenitors residing in a simple sphere, the otocyst.

8 lized to discrete axial domains in the early otocyst.

9 ogenesis but also normal neurogenesis in the otocyst.

10 otch function, was deleted in the developing otocyst.

11 racter in specific regions of the developing otocyst.

12 roliferation of the dorsolateral part of the otocyst.

13 opus, and promotes its morphogenesis into an otocyst.

14 helial cells that contributes to most of the otocyst.

15 ry domain in the embryonic chicken and mouse otocyst.

16 e and promotes dorsal cell identities in the otocyst.

17 pit, before spreading throughout the dorsal otocyst.

18 , Dlx5 and Wnt2b in the dorsal region of the otocyst.

19 pressing activated Notch (NICD) in the chick otocyst.

20 ch pinches off as a small vesicle called the otocyst.

21 todermal placode that invaginates to form an otocyst.

22 or otic induction or early patterning of the otocyst.

23 gionalized expression pattern throughout the otocyst.

24 and sensory organ fate specification in the otocyst.

25 is expressed in the macula of the developing otocyst.

26 re expressed in the epithelial layers of the otocyst.

27 significant number of embryos failed to form otocysts.

28 of the ChR-2 gene into the developing murine otocyst, 2) expression of ChR-2(H134R) in an auditory ce

29 undaries intersect at the dorsal pole of the otocyst, a convergence that may be critical for the spec

30 Conditional knockout and null otocysts also had reductions in vestibulo-cochlear gangl

31 The otocyst, an anlage of the inner ear, presents an attract

32 ert non-neuronal epithelial cells within the otocyst and cochlea as well as the 3T3 fibroblast cells

33 ect comparisons of the early human embryonic otocyst and fetal sensory organs with human IEOs.

34 minate from the anterior ventral part of the otocyst and form the cochleovestibular ganglion of the i

35 Dlx3 expression then resolves to the dorsal otocyst and gradually becomes limited to the endolymphat

36 estrict neurogenesis to the anterior-ventral otocyst and implicate another T-box factor, TBX1, as a c

37 prevalent in the epithelium of the otic pit, otocyst and membranous labyrinth as they underwent morph

38 on 382 individual cells from the developing otocyst and neuroblast lineages to assay 96 genes repres

39 events requires the normal formation of the otocyst and sensory maculae, specific secretion and loca

40 m cells in different parts of the placode or otocyst and that cell mixing plays a large role in ear d

41 trate our method, we used cells of the mouse otocyst and the renal vesicle as examples.

42 enitors express NEUROG1, delaminate from the otocyst, and coalesce to form the neurons that innervate

43 in this region as the pit closes to form the otocyst, and distinct boundaries become defined along th

44 reaction (RT-PCR) in murine tissue sections, otocyst, and ganglion explants.

45 ified, delaminate from the epithelium of the otocyst, and migrate to form the auditory-vestibular gan

46 phorin3a (Sema3a) is expressed in the dorsal otocyst, and Sema3a mutant mice show defects in afferent

47 nd expansion of the dorsolateral wall of the otocyst, and showed that this process is generated by ch

48 ally present throughout the otic placode and otocyst, and then it becomes progressively restricted to

49 inate from this islet-1-positive zone of the otocyst, and these neurons maintain islet-1 expression u

50 and Wnt3a, are incorrectly expressed in VAD otocysts, and the sensory patches and vestibulo-acoustic

51 in ventral and lateral regions of Tbx2/3cDKO otocysts around E10.5.

52 r cell precursors and throughout the growing otocyst as it functions through proliferation or its lat

53 dy presents such an analysis for the chicken otocyst at stages 13-29 (embryonic days 2.5-6).

54 monophasic pulse into Connexin30(-/-) mouse otocysts at embryonic day 11.5, is able to prevent putat

55 nsion of the neurogenic domain in Tbx2/3cDKO otocysts at this stage.

56 ear arises independently in the rudimentary otocyst based on Bone morphogenetic protein 4 (Bmp4) exp

57 Prox1 is expressed in the otocyst beginning at embryonic day (E)11, in the develop

58 enous Noggin was delivered to the developing otocyst by using a replication-competent avian retroviru

59 ows that all regions of the otic placode and otocyst can give rise to the sensory organs of the inner

60 In Lmo4-null otocysts, canal outpouches failed to form and cell proli

61 urn is related to a down-regulation of early otocyst cell proliferation.

62 that this process is generated by changes in otocyst cell shape from columnar to squamous, as opposed

63 and resemblance to mouse embryonic day 10.5 otocyst cells implied reasonable robustness of the guida

64 tion of MSCs with embryonic hindbrain/somite/otocyst conditioned medium or prenatal cochlea explants

65 Immunohistochemistry applied to otocyst cultures in the absence of glia revealed that ne

66 Since the superior part of the otocyst demonstrates outward expansion that is comparabl

67 component of the previously uncharacterized otocyst-derived factor, which directs initial neurite ou

68 Otocyst-derived ganglia exhibit rapid neuron-specific mi

69 We have investigated the fate of the otocyst-derived inner ear sensory neurons in the absence

70 shown to be essential for the development of otocyst-derived inner ear sensory neurons.

71 play a role in neurogenesis, is expressed in otocyst-derived neural precursor cells and later in the

72 The inner ear consists of two otocyst-derived, structurally and functionally distinct

73 omeobox transcription factor, cProx1, during otocyst development in chickens.

74 ic abnormalities, Tbx1 is expressed early in otocyst development in the otic epithelium and in the pe

75 The simple primordium of the inner ear (otocyst) differentiates into many cell types, including

76 F-3 is required only in the later process of otocyst differentiation.

77 derived from defined compartments within the otocyst during embryogenesis.

78 sion of miR-96 or miR-182 induces duplicated otocysts, ectopic or expanded sensory patches, and extra

79 To address this issue, each axis of the otocyst (embryonic day 2.5, E2.5, stage 16-17) was chang

80 d after deafening by surgical removal of the otocyst (embryonic precursor of the inner ear) or colume

81 onal differences in proliferation within the otocyst epithelium that are more complex than previously

82 We show that in the mouse otocyst epithelium, Tbx1 suppresses neurogenin 1-mediate

83 sion during the initial morphogenesis of the otocyst epithelium.

84 narrow ventromedial band of the rudimentary otocyst, extending between its rostral and caudal poles.

85 ated by Sox10, Twist, and Foxd3 and inhibits otocyst formation and otic expression of Sox10 and Eya1.

86 nitor the cellular movements associated with otocyst formation and to aid in interpreting the changin

87 The otocyst harbors progenitors for most cell types of the m

88 s further show that the inferior part of the otocyst has a high level of proliferation, whereas the s

89 acode induction and early development of the otocyst; however, the results of experiments in mouse an

90 a LIM-HD protein, is expressed early in the otocyst in the region that gives rise to both the audito

91 established a three-dimensional model of the otocyst in which each individual cell can be precisely m

92 sl1 is expressed in the prosensory region of otocyst, in young hair cells and supporting cells, and i

93 controls the development of the dorsolateral otocyst into semicircular canals and cristae through two

94 estriction of Wnt target genes to the dorsal otocyst is also influenced by Shh.

95 t thinning and expansion of the dorsolateral otocyst is regulated by BMP/SMAD signaling, which is bot

96 increased cell death in the early developing otocyst, leading to a decreased size and malformation of

97 Ablation of Tbx2 from the otocyst led to cochlear hypoplasia, whereas loss of Tbx3

98 ing otic tissue expresses exclusively dorsal otocyst markers.

99 The otic vesicle (otocyst) occupies a pivotal position in inner ear develo

100 gmentation of E-cadherin in the dorsolateral otocyst, occurring concomitantly with cell shape change,

101 lementation of the target gene cDNA into the otocysts of homozygous Slc24a4 knockout mice significant

102 NM) that follows surgical destruction of the otocyst on E3, a procedure that deafferents NM neurons b

103 ormed after injecting virus into the chicken otocyst on embryonic days 2.5-5.5.

104 he otic placode, growth of the otic vesicle (otocyst), otolith formation, morphogenesis of the semici

105 cytokine that is released by the developing otocyst, plays a role in regulating early innervation of

106 The dual role of Six1a in the developing otocyst provides a mechanism for balancing the relative

107 initial dorsal-specific morphogenesis of the otocyst, providing new information about how regional mo

108 During development of the otocyst, regional morphogenesis establishes a dorsal ves

109 causes dysregulation of neural competence in otocyst regions linked to the formation of either mechan

110 reas the initial compartmentalization of the otocyst remains unaffected.

111 Neither unilateral nor bilateral otocyst removal caused detectable changes in the intensi

112 ell population has established itself in the otocyst, restores marker expression lost in germ line mu

113 on of Notch by cDNA electroporation in chick otocysts results in formation of ectopic sensory patches

114 ttern of expression occurs just prior to the otocyst's transition to a more complex three-dimensional

115 de RNA-sequencing and CUT&Tag studies in the otocyst show that CHD7 regulates Sox2 expression and act

116 nstrated and this resulted in a reduction of otocyst size together with reduction in expression of ea

117 nction blocks inner ear development at early otocyst stage and after neurogenesis.

118 We used a Cre driver to delete Ebf1 at the otocyst stage before development of the cochlea.

119 At the otocyst stage, Bmp4 is expressed in each presumptive sen

120 By the otocyst stage, the expression of both L-fng and Ser1 lar

121 y arrest of the inner ear development at the otocyst stage.

122 SOX2 deficiency at otocyst stages caused a near-absence of NEUROG1-expressi

123 At otocyst stages the two genes define a broad lateral doma

124 Xenopus laevis inner ear at otic placode and otocyst stages to determine the developmental origins of

125 During otocyst stages, SOX2 shifted dramatically from a lateral

126 ession is maintained at the otic pit and the otocyst stages.

127 of these genes is affected in the Hmx2 null otocyst suggesting a complex regulatory role for Hmx2 in

128 mains, Znf703 is selectively absent from the otocyst, suggesting that Znf703 must be specifically cle

129 and as well as in regions of the developing otocyst that are mainly fated to give rise to sensory ce

130 Tbx1 null mutants have a small otocyst that fails to grow and remodel and does not give

131 Our findings show that regions of the otocyst that give rise to neurons or hair cells are dist

132 enchymal cells surrounding the region of the otocyst that is destined to form the semicircular canals

133 rge from epithelial outgrowths of the dorsal otocyst, the central regions of which fuse and resorb to

134 nd Notch activity to the ventral half of the otocyst, thereby positioning the neurosensory competent

135 of the dorsal portion (pars superior) of the otocyst to a fully developed vestibular system.

136 nd morphogenesis of the pars superior of the otocyst to form a complex labyrinth of cavities and duct

137 s well as outgrowth and restructuring of the otocyst to form a complex labyrinth.

138 cochlea emerges from the ventral pole of the otocyst to form a one and three-quarter coil.

139 nditional deletion of Chd7 in the developing otocyst using Foxg1-Cre resulted in cochlear hypoplasia

140 e the posteroventral rim becomes the lateral otocyst wall.

141 genes within the Rac1(CKO); Rac3(-/-) mutant otocyst was largely normal, however, indicating that Rac

142 d loss-of-function approaches in the chicken otocyst, we show that these early changes in Sox2 expres

143 aling pathway regulators to developing chick otocysts, we show that BMP signaling regulates the expre

144 prosensory epithelial cells in the anterior otocyst, where they are diverted into a neuroblast fate

145 , and Dlx5 in the dorsolateral domain of the otocyst, whereas the initial compartmentalization of the

146 brain is required to induce formation of the otocyst, while the latter imply that FGF-3 is required o