Mesenchymal derivatives from the neural crest.

Nakamura, Harukazu

doi:10.1679/aohc.45.127

Cited by 29 publications

(14 citation statements)

References 28 publications

(23 reference statements)

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“…The smooth muscle walls of the great arteries are normally formed by NCCs (Jiang et al, 2000; Nakamura, 1982), whereas those surrounding the dorsal aortas are of mesodermal origin. Like the great arteries of the controls, the aberrant vessels in mutants were also surrounded by wall containing smooth muscle alpha-actin (SMα–A)-positive cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

Neural crest cell-specific deletion of Rac1 results in defective cell–matrix interactions and severe craniofacial and cardiovascular malformations

Thomas

Kim

Núñez

et al. 2010

Developmental Biology

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The small GTP-binding protein Rac1, a member of the Rho family of small GTPases, has been implicated in regulation of many cellular processes including adhesion, migration and cytokinesis. These functions have largely been attributed to its ability to reorganize cytoskeleton. While the function of Rac1 is relatively well known in vitro, its role in vivo has been poorly understood. It has previously been shown that in neural crest cells (NCCs) Rac1 is required in a stage-specific manner to acquire responsiveness to mitogenic EGF signals. Here we demonstrate that mouse embryos lacking Rac1 in neural crest cells (Rac1/Wnt1-Cre) showed abnormal craniofacial development including regional ectodermal detachment associated with mesenchymal acellularity culminating in cleft face at E12. Rac1/Wnt1-Cre mutants also displayed inappropriate remodelling of pharyngeal arch arteries and defective outflow tract septation resulting in the formation of a common arterial trunk (‘persistent truncus arteriosus’ or PTA). The mesenchyme around the aortic sac also developed acellular regions, and the distal aortic sac became grossly dysmorphic, forming a pair of bilateral, highly dilated arterial structures connecting to the dorsal aortas. Smooth muscle cells lacking Rac1 failed to differentiate appropriately, and subpopulations of post-migratory NCCs demonstrated aberrant cell death and attenuated proliferation. These novel data demonstrate that while Rac1 is not required for normal NCC migration in vivo, it plays a critical cell-autonomous role in post-migratory NCCs during craniofacial and cardiac development by regulating the integrity of the craniofacial and pharyngeal mesenchyme.

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Section: Resultsmentioning

confidence: 99%

Neural crest cell-specific deletion of Rac1 results in defective cell–matrix interactions and severe craniofacial and cardiovascular malformations

Thomas

Kim

Núñez

et al. 2010

Developmental Biology

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“…26 Basic differences in the ectomesenchyme in various regions of the pharyngeal arches have been described 27. The genes responsible for tetralogy of Fallot and PA–VSD in del22q and non-del22q patients may have different effects on the development of neural crest derived populations.…”

Section: Discussionmentioning

confidence: 99%

Relation of genotype 22q11 deletion to phenotype of pulmonary vessels in tetralogy of Fallot and pulmonary atresia-ventricular septal defect

Chessa

Butera

Bonhoeffer

et al. 1998

Heart

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“…1979;Johnston et al . 1979;Meier 1982;Nakamura 1982). More recently, extensive research in avian embryos (Creuzet et al .…”

Section: Introductionmentioning

confidence: 99%

Abnormal migration and distribution of neural crest cells in Pax6 heterozygous mutant eye, a model for human eye diseases

et al. 2006

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Mesenchymal derivatives from the neural crest.

Cited by 29 publications

References 28 publications

Neural crest cell-specific deletion of Rac1 results in defective cell–matrix interactions and severe craniofacial and cardiovascular malformations

Neural crest cell-specific deletion of Rac1 results in defective cell–matrix interactions and severe craniofacial and cardiovascular malformations

Relation of genotype 22q11 deletion to phenotype of pulmonary vessels in tetralogy of Fallot and pulmonary atresia-ventricular septal defect

Abnormal migration and distribution of neural crest cells in Pax6 heterozygous mutant eye, a model for human eye diseases

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