Signalling from hindbrain boundaries regulates neuronal clustering that patterns neurogenesis

Terriente, Javier; Gerety, Sebastian S.; Watanabe-Asaka, Tomomi; González‐Quevedo, Rosa; Wilkinson, David G.

doi:10.1242/dev.080135

Cited by 44 publications

(51 citation statements)

References 45 publications

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“…Furthermore, EGFP expression in rhombomere neurons at the prim-15 stage (Fig. S4C) is also consistent with the previously reported pattern of fgf20a expression (Terriente et al, 2012). Taken together, these data supported the notion that fgf20a expression during fin regeneration is recapitulated by the enhancer trap zebrafish line, and that Fgf20a is an Fgf ligand that is locally expressed in the basal layer of the wound epidermis.…”

Section: The Fgf Ligands That Are Expressed During Fin Regenerationsupporting

confidence: 91%

Fgf signalling controls diverse aspects of fin regeneration

et al. 2016

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Studies have shown that fibroblast growth factor (Fgf ) signalling is necessary for appendage regeneration, but its exact function and the ligands involved during regeneration have not yet been elucidated. Here, we performed comprehensive expression analyses and identified fgf20a and fgf3/10a as major Fgf ligands in the wound epidermis and blastema, respectively. To reveal the target cells and processes of Fgf signalling, we performed a transplantation experiment of mesenchymal cells that express the dominantnegative Fgf receptor 1 (dnfgfr1) under control of the heat-shock promoter. This mosaic knockdown analysis suggested that Fgf signalling is directly required for fin ray mesenchyme to form the blastema at the early pre-blastema stage and to activate the regenerative cell proliferation at a later post-blastema stage. These results raised the possibility that the early epidermal Fgf20a and the later blastemal Fgf3/10a could be responsible for these respective processes. We demonstrated by gain-of-function analyses that Fgf20a induces the expression of distal blastema marker junbl, and that Fgf3 promotes blastema cell proliferation. Our study highlights that Fgfs in the wound epidermis and blastema have distinct functions to regulate fin regeneration cooperatively.

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Section: The Fgf Ligands That Are Expressed During Fin Regenerationsupporting

confidence: 91%

Fgf signalling controls diverse aspects of fin regeneration

et al. 2016

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“…Sema3fb and sema3gb are also expressed at the hindbrain rhombomere boundaries. When Terriente and colleagues knocked down sema3fb and sema3gb or nrp2a using morpholinos, they found reduced clustering of fgf20a‐ expressing neurons in the rhombomeres (Terriente, Gerety, Watanabe‐Asaka, Gonzalez‐Quevedo, & Wilkinson, ). The authors propose a model in which fgf20a ‐expressing neurons also express the nrp2a receptor and are restricted from migrating away from the center of the rhombomere by repulsive sema3fb and sema3gb at the rhombomere boundaries.…”

Section: Discussionmentioning

confidence: 99%

Expression of class III Semaphorins and their receptors in the developing chicken (Gallus gallus) inner ear

Scott¹,

Jia²,

Biesemeier³

et al. 2019

J of Comparative Neurology

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Class III Semaphorin (Sema) secreted ligands are known to repel neurites expressing Neuropilin (Nrp) and/or Plexin (Plxn) receptors. There is, however, a growing body of literature supporting that Sema signaling also has alternative roles in development such as synaptogenesis, boundary formation, and vasculogenesis. To evaluate these options during inner ear development, we used in situ hybridization or immunohistochemistry to map the expression of Sema3D, Sema3F, Nrp1, Nrp2, and PlxnA1 in the chicken (Gallus gallus) inner ear from embryonic day (E)5–E10. The resulting expression patterns in either the otic epithelium or its surrounding mesenchyme suggest that Sema signaling could be involved in each of the varied functions reported for other tissues. Sema3D expression flanking the sensory tissue in vestibular organs suggests that it may repel Nrp2‐ and PlxnA1‐expressing neurites of the vestibular ganglion away from nonsensory epithelia, thus channeling them into the sensory domains at E5–E8. Expression of Sema signaling genes in the sensory hair cells of both the auditory and vestibular organs on E8–E10 may implicate Sema signaling in synaptogenesis. In the nonsensory regions of the cochlea, Sema3D in the future tegmentum vasculosum opposes Nrp1 and PlxnA1 in the future cuboidal cells; the abutment of ligand and receptors in adjacent domains may enforce or maintain the boundary between them. In the mesenchyme, Nrp1 colocalized with capillary‐rich tissue. Sema3D immediately flanks this Nrp1‐expressing tissue, suggesting a role in endothelial cell migration towards the inner ear. In summary, Sema signaling may play multiple roles in the developing inner ear.

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“…In chick, it has been demonstrated that border cells include a population of Sox2‐expressing neural progenitor cells that give rise to neurons of both adjacent rhombomeres (Peretz et al, ). In zebrafish, these boundary cells express the chemorepellants Sema3fb and Sema3gb, which are critical for maintaining the positioning of Nrp2a‐expressing neuronal populations within the rhombomere (Terriente, Gerety, Watanabe‐Asaka, Gonzalez‐Quevedo, & Wilkinson, ). Boundary cells may help to determine cell affinity properties that drive the proper segregation of more differentiated rhombomere cells.…”

Section: Rhombomere Organization and Mechanisms Of Segregationmentioning

confidence: 99%

Cellular organization and boundary formation in craniofacial development

Kindberg

Bush

2019

Genesis

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Summary Craniofacial morphogenesis is a highly dynamic process that requires changes in the behaviors and physical properties of cells in order to achieve the proper organization of different craniofacial structures. Boundary formation is a critical process in cellular organization, patterning, and ultimately tissue separation. There are several recurring cellular mechanisms through which boundary formation and cellular organization occur including, transcriptional patterning, cell segregation, cell adhesion and migratory guidance. Disruption of normal boundary formation has dramatic morphological consequences, and can result in human craniofacial congenital anomalies. In this review we discuss boundary formation during craniofacial development, specifically focusing on the cellular behaviors and mechanisms underlying the self‐organizing properties that are critical for craniofacial morphogenesis.

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Signalling from hindbrain boundaries regulates neuronal clustering that patterns neurogenesis

Cited by 44 publications

References 45 publications

Fgf signalling controls diverse aspects of fin regeneration

Fgf signalling controls diverse aspects of fin regeneration

Expression of class III Semaphorins and their receptors in the developing chicken (Gallus gallus) inner ear

Cellular organization and boundary formation in craniofacial development

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