Developmental relations between sixth nerve motor neurons and their targets in the chick embryo

Wahl, Christina; Noden, Drew M.; Baker, R.

doi:10.1002/aja.1002010209

Cited by 52 publications

(44 citation statements)

References 46 publications

(42 reference statements)

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“…It is not known when during the extended period of morphogenesis each muscle acquires its positional and molecular identity. Examination of early projections by motor axons suggests that cranial nerves III and VI can discriminate among alternate targets when muscle primordia are still at their early condensation phases (Wahl et al, 1994), suggesting that identity may be established within or around myoblast aggregation sites, as has been suggested for appendicular muscles (Duprez et al, 1999;Kardon et al, 2003).…”

Section: Muscle Originsmentioning

confidence: 89%

Spatial relations between avian craniofacial neural crest and paraxial mesoderm cells

Evans

Noden

2006

Developmental Dynamics

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161

177

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Fate maps based on quail-chick grafting of avian cephalic neural crest precursors and paraxial mesoderm cells have identified the majority of derivatives from each population but have not unequivocally resolved the precise locations of and population dynamics at the interface between them. The relation between these two mesenchymal tissues is especially critical for the development of skeletal muscles, because crest cells play an essential role in their differentiation and subsequent spatial organization. It is not known whether myogenic mesoderm and skeletogenic neural crest cells establish permanent relations while en route to their final destinations, or later at the sites where musculoskeletal morphogenesis is completed. We applied ␤-galactosidase-encoding, replication-incompetent retroviruses to paraxial mesoderm, to crest progenitors, or at the interface between mesodermal and overlying neural crest as both were en route to branchial or periocular regions in chick embryos. With respect to skeletal structures, the results identify the avian neural crest:mesoderm boundary at the junction of the supraorbital and calvarial regions of the frontal bone, lateral to the hypophyseal foramen, and rostral to laryngeal cartilages.

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Section: Muscle Originsmentioning

confidence: 89%

Spatial relations between avian craniofacial neural crest and paraxial mesoderm cells

Evans

Noden

2006

Developmental Dynamics

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161

177

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“…6, 7; see also Fig. 10;Wahl et al, 1994;Evans and Noden, 2006). These studies identified progenitors for endothelial cells, smooth muscles, and a wide range of connective tissues in addition to skeletal muscles within paraxial mesoderm.…”

Section: Paraxial Mesodermmentioning

confidence: 99%

“…17). These populations of myogenic cells, often already including multinucleated myotubes (Wahl et al, 1994), move en masse into neural crest-occupied periocular territories (Wahl and Noden, 1997;Creuzet et al, 2005). Migration of single cells does not occur and these myoblasts do not express the c-Met receptor.…”

Section: Morphogenesis Of Head Musclesmentioning

confidence: 99%

“…The diversity of relocation strategies is exemplified by (1) the migration of individual myoblasts into the limbs and facial regions, (2) expansions of sheets or cords of myogenic precursors (e.g., muscle buds, Christ and Ordahl, 1995;Burke and Nowicki, 2003) to form hypaxial body wall and branchial arch muscles, and (3) translocations of condensed cohorts of differentiating muscle cells as seen during EOM development (Wahl et al, 1994). In some cases, e.g., tongue muscles and the diaphragm, a combination of these strategies is likely employed.…”

Section: Morphogenesis Of Head Musclesmentioning

confidence: 99%

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The differentiation and morphogenesis of craniofacial muscles

Noden

Francis‐West

2006

Developmental Dynamics

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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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“…We found that the abducens nerve first projects to the LR on embryonic day 4 (E4) (8,9) (Fig. 1A), whereas the trochlear and the OMN reach the DO and VO, respectively, on E5 (Fig.…”

mentioning

confidence: 97%

Axon guidance in the developing ocular motor system and Duane retraction syndrome depends on Semaphorin signaling via alpha2-chimaerin

Ferrario

Baskaran

Clark

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Eye movements depend on correct patterns of connectivity between cranial motor axons and the extraocular muscles. Despite the clinical importance of the ocular motor system, little is known of the molecular mechanisms underlying its development. We have recently shown that mutations in the Chimaerin-1 gene encoding the signaling protein α2-chimaerin (α2-chn) perturb axon guidance in the ocular motor system and lead to the human eye movement disorder, Duane retraction syndrome (DRS). The axon guidance cues that lie upstream of α2-chn are unknown; here we identify candidates to be the Semaphorins (Sema) 3A and 3C, acting via the PlexinA receptors. Sema3A/C are expressed in and around the developing extraocular muscles and cause growth cone collapse of oculomotor neurons in vitro. Furthermore, RNAi knockdown of α2-chn or PlexinAs in oculomotor neurons abrogates Sema3A/C-dependent growth cone collapse. In vivo knockdown of endogenous PlexinAs or α2-chn function results in stereotypical oculomotor axon guidance defects, which are reminiscent of DRS, whereas expression of α2-chn gain-of-function constructs can rescue PlexinA loss of function. These data suggest that α2-chn mediates Sema3-PlexinA repellent signaling. We further show that α2-chn is required for oculomotor neurons to respond to CXCL12 and hepatocyte growth factor (HGF), which are growth promoting and chemoattractant during oculomotor axon guidance. α2-chn is therefore a potential integrator of different types of guidance information to orchestrate ocular motor pathfinding. DRS phenotypes can result from incorrect regulation of this signaling pathway.

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Developmental relations between sixth nerve motor neurons and their targets in the chick embryo

Cited by 52 publications

References 46 publications

Spatial relations between avian craniofacial neural crest and paraxial mesoderm cells

Spatial relations between avian craniofacial neural crest and paraxial mesoderm cells

The differentiation and morphogenesis of craniofacial muscles

Axon guidance in the developing ocular motor system and Duane retraction syndrome depends on Semaphorin signaling via alpha2-chimaerin

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