Migration of cranial neural crest cells to the pharyngeal arches and heart in rat embryos

Fukiishi, Yonetaka; Morriss‐Kay, Gillian M.

doi:10.1007/bf00338048

Cited by 106 publications

(62 citation statements)

References 29 publications

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“…Recent studies have shown, however, that some precursors of the OFT endocardium and mesenchyme (but not those of the AV endocardium) migrate to the heart via the cephalic paraxial and lateral mesoderm (Noden, 1991). Furthermore, experiments conducted with chick-quail chimeras (Phillips et al, 1987) and in rat embryos (Fukiishi and Morriss-Kay, 1992) have demonstrated that cells from the neural crest at the level of the first three to four occipital somites also enter the cushion tissue of the OFT. No neural crest contribution has been identified in the AV region.…”

Section: Msx-i Expression In Cushion Tissue Of the Oftmentioning

confidence: 99%

Expression of homeobox genes Msx‐1 (Hox‐7) and Msx‐2 (Hox‐8) during cardiac development in the chick

Chan-Thomas¹,

Thompson

Robert

et al. 1993

Developmental Dynamics

156

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The vertebrate homeobox genes Msx-1 and Msx-2 are related to the Drosophila msh gene and are expressed in a variety of tissues during embryogenesis. We have examined their expression by in situ hybridisation during critical stages of cardiac development in the chick from stages 15 + to 37. Msx-1 expression is apparent in a number of non-myocardial cell populations, including cells undergoing an epithelial to mesenchymal transformation in the atrioventricular and the outflow tract regions that play an integral role in heart septation and valve formation. Msx-2 expression is restricted to a distinct subpopulation of myocardial cells that, in later stages, coincides morphologically with the cardiac conduction system. The timing of Msx-2 expression suggests that it plays a role in conduction system tissue formation and that it identifies precursor cells of this specialised myocardium. The pattern of Msx-2 expression is discussed with reference to current models of conduction tissue development. 0 1993 Wiley-Liss, Inc.

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Section: Msx-i Expression In Cushion Tissue Of the Oftmentioning

confidence: 99%

Expression of homeobox genes Msx‐1 (Hox‐7) and Msx‐2 (Hox‐8) during cardiac development in the chick

Chan-Thomas¹,

Thompson

Robert

et al. 1993

Developmental Dynamics

156

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“…Most of the bone and cartilage in the craniofacial region arises from transient structures called pharyngeal arches (Fukiishi andMorriss-Kay, 1992, Bronner-Fraser, 1995), which are populated by cranial neural crest cells (NCCs). These NCCs migrate from the neuroectoderm of the posterior midbrain and hindbrain to the arches while undergoing an epithelial to mesenchymal transition (Le Douarin, 1982, Tosney, 1982.…”

Section: Introductionmentioning

confidence: 99%

Fate of cranial neural crest cells during craniofacial development in endothelin-A receptor-deficient mice

Abe¹,

Ruest²,

Clouthier³

2007

Int. J. Dev. Biol.

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Most of the bone, cartilage and connective tissue of the lower jaw is derived from cranial neural crest cells (NCCs) arising from the posterior midbrain and hindbrain. Multiple factors direct the patterning of these NCCs, including endothelin-1-mediated endothelin A receptor (Edn1/Ednra) signaling. Loss of Ednra signaling results in multiple defects in lower jaw and neck structures, including homeotic transformation of lower jaw structures into upper jawlike structures. However, since the Ednra gene is expressed by both migrating and post-migrating NCCs, the actual function of Ednra in cranial NCC development is not clear. Ednra signaling could be required for normal migration or guidance of NCCs to the pharyngeal arches or in subsequent events in post-migratory NCCs, including proliferation and survival. To address this question, we performed a fate analysis of cranial NCCs in Ednra-/-embryos using the R26R;Wnt1-Cre reporter system, in which Cre expression within NCCs results in permanent β-galactosidase activity in NCCs and their derivatives. We find that loss of Ednra does not detectably alter either migration of most cranial NCCs into the mandibular first arch and second arch or their subsequent proliferation. However, mesenchymal cell apoptosis is increased two fold in both E9.5 and E10.5 Ednra-/-embryos, with apoptotic cells being present in and just proximal to the pharyngeal arches. Based on these studies, Ednra signaling appears to be required by most cranial NCCs after they reach the pharyngeal arches. However, a subset of NCCs appear to require Ednra signaling earlier, with loss of Ednra signaling likely leading to premature cessation of migration into or within the arches and subsequent cell death.

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“…Most notably, chickens have a right-sided aortic arch, bilateral ducti arteriosi, and bilateral brachiocephalic arteries (Brown and Baldwin, 2006). Cell labeling and fate mapping experiments in mice (Waldo et al, 1999;Yamauchi et al, 1999;Jiang et al, 2000;Li et al, 2000;Pietri et al, 2003) and rat (Fukiishi and Morriss-Kay, 1992) suggest a conservation of function of the neural crest in mammalian cardiovascular development. There are also multiple genetic and teratogenic alterations in mouse and human that result in a similar phenotype to that of chick neural crest ablation (NCA).…”

Section: Introductionmentioning

confidence: 99%

Temporal–spatial ablation of neural crest in the mouse results in cardiovascular defects

Porras

Brown

2007

Developmental Dynamics

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Neural crest cells are thought to play a critical role in human conotruncal morphogenesis and dysmorphogenesis. Much of our understanding of the contribution of neural crest to cardiovascular patterning comes from ablation and transplantation experiments in avian species. Although fate mapping experiments in mice suggests a conservation of function, the functional requirement for neural crest in cardiovascular development in mammals has not been formally tested. We used a novel two component genetic system for the temporal-spatial ablation of neural crest in the mouse. Affected embryos displayed a spectrum of cardiovascular outflow tract defects and aortic arch patterning abnormalities. We show that the severity of the cardiovascular phenotype is directly related to the level and extent of neural crest ablation. This is the first report of cardiac neural crest ablation in mammals, and it provides important insight into the role of the mammalian neural crest during cardiovascular development. Developmental Dynamics 237:153-162, 2008.

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Migration of cranial neural crest cells to the pharyngeal arches and heart in rat embryos

Cited by 106 publications

References 29 publications

Expression of homeobox genes Msx‐1 (Hox‐7) and Msx‐2 (Hox‐8) during cardiac development in the chick

Expression of homeobox genes Msx‐1 (Hox‐7) and Msx‐2 (Hox‐8) during cardiac development in the chick

Fate of cranial neural crest cells during craniofacial development in endothelin-A receptor-deficient mice

Temporal–spatial ablation of neural crest in the mouse results in cardiovascular defects

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