Establishing the trochlear motor axon trajectory: role of the isthmic organiser and Fgf8

Irving, Carol; Malhas, Amar; Guthrie, Sarah; Mason, Ivor

doi:10.1242/dev.00117

Cited by 58 publications

(57 citation statements)

References 68 publications

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“…1 B). Although FGF8 acts as a guidance cue (Irving et al, 2002;Shirasaki et al, 2006), the fact that FGF8-beads did not repel mDAN axons (supplemental Fig. 8, available at www.…”

Section: Discussionmentioning

confidence: 99%

FGF8 Signaling Regulates Growth of Midbrain Dopaminergic Axons by Inducing Semaphorin 3F

Yamauchi¹,

Mizushima²,

Tamada³

et al. 2009

J. Neurosci.

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Accumulating evidence indicates that signaling centers controlling the dorsoventral (DV) polarization of the neural tube, the roof plate and the floor plate, play crucial roles in axon guidance along the DV axis. However, the role of signaling centers regulating the rostrocaudal (RC) polarization of the neural tube in axon guidance along the RC axis remains unknown. Here, we show that a signaling center located at the midbrain-hindbrain boundary (MHB) regulates the rostrally directed growth of axons from midbrain dopaminergic neurons (mDANs). We found that beads soaked with fibroblast growth factor 8 (FGF8), a signaling molecule that mediates patterning activities of the MHB, repelled mDAN axons that extended through the diencephalon. This repulsion may be mediated by semaphorin 3F (sema3F) because (1) FGF8-soaked beads induced an increase in expression of sema3F, (2) sema3F expression in the midbrain was essentially abolished by the application of an FGF receptor tyrosine kinase inhibitor, and (3) mDAN axonal growth was also inhibited by sema3F. Furthermore, mDAN axons expressed a sema3F receptor, neuropilin-2 (nrp2), and the removal of nrp-2 by gene targeting caused caudal growth of mDAN axons. These results indicate that the MHB signaling center regulates the growth polarity of mDAN axons along the RC axis by inducing sema3F.

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“…1 B). Although FGF8 acts as a guidance cue (Irving et al, 2002;Shirasaki et al, 2006), the fact that FGF8-beads did not repel mDAN axons (supplemental Fig. 8, available at www.…”

Section: Discussionmentioning

confidence: 99%

FGF8 Signaling Regulates Growth of Midbrain Dopaminergic Axons by Inducing Semaphorin 3F

Yamauchi¹,

Mizushima²,

Tamada³

et al. 2009

J. Neurosci.

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“…12). In these contexts, however, HGF acts as a chemoattractant for outgrowing motor axons (Irving et al, 2002). C-Met loss-of-function studies reveal a key role for this signaling pathway in the formation of the muscles of facial expression, e.g., the orbicularis, buccinator, and platysma (Prunotto et al, 2004), in addition to most (but not all) tongue muscles.…”

Section: Molecular Biographies Of Developing Head Musclesmentioning

confidence: 99%

The differentiation and morphogenesis of craniofacial muscles

Noden

Francis‐West

2006

Developmental Dynamics

355

358

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Unraveling the complex tissue interactions necessary to generate the structural and functional diversity present among craniofacial muscles is challenging. These muscles initiate their development within a mesenchymal population bounded by the brain, pharyngeal endoderm, surface ectoderm, and neural crest cells. This set of spatial relations, and in particular the segmental properties of these adjacent tissues, are unique to the head. Additionally, the lack of early epithelialization in head mesoderm necessitates strategies for generating discrete myogenic foci that may differ from those operating in the trunk. Molecular data indeed indicate dissimilar methods of regulation, yet transplantation studies suggest that some head and trunk myogenic populations are interchangeable. The first goal of this review is to present key features of these diversities, identifying and comparing tissue and molecular interactions regulating myogenesis in the head and trunk. Our second focus is on the diverse morphogenetic movements exhibited by craniofacial muscles. Precursors of tongue muscles partly mimic migrations of appendicular myoblasts, whereas myoblasts destined to form extraocular muscles condense within paraxial mesoderm, then as large cohorts they cross the mesoderm:neural crest interface en route to periocular regions. Branchial muscle precursors exhibit yet another strategy, establishing contacts with neural crest populations before branchial arch formation and maintaining these relations through subsequent stages of morphogenesis. With many of the prerequisite stepping-stones in our knowledge of craniofacial myogenesis now in place, discovering the cellular and molecular interactions necessary to initiate and sustain the differentiation and morphogenesis of these neglected craniofacial muscles is now an attainable goal.

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“…DIG probes were detected using NBT:BCIP (Roche); FITC probes were detected using FAST TR/Naphtol AS-MX solution (Sigma). Embryos were fixed in 4% paraformaldehyde for 20 minutes before immunohistochemistry as previously described (Irving et al, 2002). Rabbit anti-eGFP antiserum (Clontech) was used at 1:1000.…”

Section: In Situ Hybridisation and Immunohistochemistrymentioning

confidence: 99%

Notch signalling stabilises boundary formation at the midbrain-hindbrain organiser

et al. 2011

Self Cite

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The midbrain-hindbrain interface gives rise to a boundary of particular importance in CNS development as it forms a local signalling centre, the proper functioning of which is essential for the formation of tectum and cerebellum. Positioning of the mid-hindbrain boundary (MHB) within the neuroepithelium is dependent on the interface of Otx2 and Gbx2 expression domains, yet in the absence of either or both of these genes, organiser genes are still expressed, suggesting that other, as yet unknown mechanisms are also involved in MHB establishment. Here, we present evidence for a role for Notch signalling in stabilising cell lineage restriction and regulating organiser gene expression at the MHB. Experimental interference with Notch signalling in the chick embryo disrupts MHB formation, including downregulation of the organiser signal Fgf8. Ectopic activation of Notch signalling in cells of the anterior hindbrain results in an exclusion of those cells from rhombomeres 1 and 2, and in a simultaneous clustering along the anterior and posterior boundaries of this area, suggesting that Notch signalling influences cell sorting. These cells ectopically express the boundary marker Fgf3. In agreement with a role for Notch signalling in cell sorting, anterior hindbrain cells with activated Notch signalling segregate from normal cells in an aggregation assay. Finally, misexpression of the Notch modulator Lfng or the Notch ligand Ser1 across the MHB leads to a shift in boundary position and loss of restriction of Fgf8 to the MHB. We propose that differential Notch signalling stabilises the MHB through regulating cell sorting and specifying boundary cell fate.

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Establishing the trochlear motor axon trajectory: role of the isthmic organiser and Fgf8

Cited by 58 publications

References 68 publications

FGF8 Signaling Regulates Growth of Midbrain Dopaminergic Axons by Inducing Semaphorin 3F

FGF8 Signaling Regulates Growth of Midbrain Dopaminergic Axons by Inducing Semaphorin 3F

The differentiation and morphogenesis of craniofacial muscles

Notch signalling stabilises boundary formation at the midbrain-hindbrain organiser

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