Gene-Regulatory Interactions in Neural Crest Evolution and Development

Meulemans, Daniel; Bronner‐Fraser, Marianne

doi:10.1016/j.devcel.2004.08.007

Cited by 410 publications

(410 citation statements)

References 104 publications

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“…1D; Mitchell et al, 1991;Arkell and Beddington, 1997). Moreover, Ap2␣ is the earliest characterized marker of presumptive NCCs (Meulemans and Bronner-Fraser, 2004), is a competence factor for neural crest induction (Luo et al, 2003), and is necessary for normal differentiation of some NCC derivatives (Schorle et al, 1996;Zhang et al, 1996;Brewer et al, 2004). Ap2␣ expression in Chrd Ϫ/Ϫ mutants is indistinguishable from wild-type (data not shown).…”

Section: Excess Neural Crest Cells Are Generated In Chrd;nog Mutantsmentioning

confidence: 96%

Endogenous bone morphogenetic protein antagonists regulate mammalian neural crest generation and survival

Anderson

Stottmann

Choi

et al. 2006

Developmental Dynamics

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We demonstrate here that Chordin and Noggin function as bone morphogenetic protein (BMP) antagonists in vivo to promote mammalian neural crest development. Using Chrd and Nog single and compound mutants, we find that Noggin has a major role in promoting neural crest formation, in which Chordin is partially redundant. BMP signaling is increased in dorsal tissues lacking Noggin and is further increased when Chordin is also absent. The early neural crest domain is expanded with decreased BMP antagonism in vivo. Noggin and Chordin also regulate subsequent neural crest cell emigration from the neural tube. However, reduced levels of these BMP antagonists ultimately result in perturbation of neural crest cell derived peripheral nervous system and craniofacial skeletal elements. Such defects reflect, at least in part, a function to limit apoptosis in neural crest cells. Noggin and Chordin, therefore, function together to regulate both the generation and survival of neural crest cells in mammalian development. Developmental Dynamics 235:2507-2520, 2006.

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Section: Excess Neural Crest Cells Are Generated In Chrd;nog Mutantsmentioning

confidence: 96%

Endogenous bone morphogenetic protein antagonists regulate mammalian neural crest generation and survival

Anderson

Stottmann

Choi

et al. 2006

Developmental Dynamics

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“…Furthermore, AP2γ has redundant activities with AP2α in neural crest induction and nonneural ectoderm derivative development [26]. Other factors such as Pax7, Msx1, Zic1, Dlx5 and AP2α were shown as neural border specifiers [30,[63][64][65][66][67][68]. During early neuralization of the chick embryo, some factors are mainly expressed in the peripheral (Pax7, Dlx5 and AP2α) or caudal (Msx1) ectoderm and the expressions of others (Zic1) partially overlaps with cSox2 expression [68].…”

Section: Discussionmentioning

confidence: 99%

AP2γ regulates neural and epidermal development downstream of the BMP pathway at early stages of ectodermal patterning

et al. 2012

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Bone morphogenetic protein (BMP) inhibits neural specification and induces epidermal differentiation during ectodermal patterning. However, the mechanism of this process is not well understood. Here we show that AP2γ, a transcription factor activator protein (AP)-2 family member, is upregulated by BMP4 during neural differentiation of pluripotent stem cells. Knockdown of AP2γ facilitates mouse embryonic stem cell (ESC) neural fate determination and impairs epidermal differentiation, whereas AP2γ overexpression inhibits neural conversion and promotes epidermal commitment. In the early chick embryo, AP2γ is expressed in the entire epiblast before HH stage 3 and gradually shifts to the putative epidermal ectoderm during HH stage 4. In the future neural plate AP2γ inhibits excessive neural expansion and it also promotes epidermal development in the surface ectoderm. Moreover, AP2γ knockdown in ESCs and chick embryos partially rescued the neural inhibition and epidermal induction effects of BMP4. Mechanistic studies showed that BMP4 directly regulates AP2γ expression through Smad1 binding to the AP2γ promoter. Taken together, we propose that during the early stages of ectodermal patterning in the chick embryo, AP2γ acts downstream of the BMP pathway to restrict precocious neural expansion in the prospective neural plate and initiates epidermal differentiation in the future epidermal ectoderm.

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“…R. Soc. B 281: 20141729 delamination and migration (figure 2b) [97,102]. Although the presence of a neural crest in ascidians has been debated [103], a recent study of Ciona embryos demonstrates that the neural crest melanocyte regulatory network pre-dated the divergence of tunicates and vertebrates, but the cooption of mesenchyme determinants, such as Twist, into neural plate ectoderm is absent (figure 2b) [104].…”

Section: (Iii) Vertebratamentioning

confidence: 99%

“…These cells migrate extensively and give rise to diverse cell lineages, including craniofacial cartilage and bone, peripheral and enteric neurons and glia, smooth muscle, and melanocytes. The gene regulatory network (GRN) underlying neural crest formation appears to be highly conserved as a vertebrate innovation (figure 2b) [97,102]. Border induction signals (BMP and Fgf ) from ventral ectoderm and underlying mesendoderm pattern dorsal ectoderm, inducing expression of neural border specifiers (Zic and Dlx).…”

Section: (Iii) Vertebratamentioning

confidence: 99%

Chordate evolution and the three-phylum system

2014

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Traditional metazoan phylogeny classifies the Vertebrata as a subphylum of the phylum Chordata, together with two other subphyla, the Urochordata (Tunicata) and the Cephalochordata. The Chordata, together with the phyla Echinodermata and Hemichordata, comprise a major group, the Deuterostomia. Chordates invariably possess a notochord and a dorsal neural tube. Although the origin and evolution of chordates has been studied for more than a century, few authors have intimately discussed taxonomic ranking of the three chordate groups themselves. Accumulating evidence shows that echinoderms and hemichordates form a clade (the Ambulacraria), and that within the Chordata, cephalochordates diverged first, with tunicates and vertebrates forming a sister group. Chordates share tadpole-type larvae containing a notochord and hollow nerve cord, whereas ambulacrarians have dipleurula-type larvae containing a hydrocoel. We propose that an evolutionary occurrence of tadpole-type larvae is fundamental to understanding mechanisms of chordate origin. Protostomes have now been reclassified into two major taxa, the Ecdysozoa and Lophotrochozoa, whose developmental pathways are characterized by ecdysis and trochophore larvae, respectively. Consistent with this classification, the profound dipleurula versus tadpole larval differences merit a category higher than the phylum. Thus, it is recommended that the Ecdysozoa, Lophotrochozoa, Ambulacraria and Chordata be classified at the superphylum level, with the Chordata further subdivided into three phyla, on the basis of their distinctive characteristics.

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Gene-Regulatory Interactions in Neural Crest Evolution and Development

Cited by 410 publications

References 104 publications

Endogenous bone morphogenetic protein antagonists regulate mammalian neural crest generation and survival

Endogenous bone morphogenetic protein antagonists regulate mammalian neural crest generation and survival

AP2γ regulates neural and epidermal development downstream of the BMP pathway at early stages of ectodermal patterning

Chordate evolution and the three-phylum system

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