ReviewPatterning of Neural Crest Derivatives in the Avian Embryo: in Vivo and in Vitro Studies
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Like a hole in the head: Development, evolutionary implications and diseases of the cranial foramina
2019, Seminars in Cell and Developmental BiologyCitation Excerpt :In contrast to the mesodermally derived axial and appendicular skeletons, the skull has contributions from the neural crest as well as somitic and cranial paraxial mesoderm [6,7]. A number of fate mapping studies using quail/chick chimeras [8,9] as well as retroviral labelling [10] have shown that the majority of the chick facial skeleton (viscerocranium) and part of the rostral frontal bone (a component of the dermatocranium) are of neural crest origin with the remaining dermatocranium being of cranial mesodermal origin (Fig. 1). Similar studies using genetic labelling of neural crest with wnt1-cre and somitic mesoderm with Mesp1-cre in mice [11–13] and zebrafish neural crest with Sox10-cre [14] have shown the conserved evolution of this pattern in other vertebrates.
Chemotaxis during neural crest migration
2016, Seminars in Cell and Developmental BiologyCitation Excerpt :NC cells receive inductive signals from the neural tube, paraxial mesoderm and the overlying ectoderm as they migrate [23]. Their specification is a multistep process; their fate is based on these paracrine signals, as well as the time at which they migrate, their origin and the stream in which they are found [23–27]. The cranial NC contributes to the craniofacial mesenchyme, which includes cartilage, bone, teeth, cranial neurons, glia and connective tissue.
Chicken trunk neural crest migration visualized with HNK1
2015, Acta HistochemicaCitation Excerpt :Importantly, neural crest cells are classified depending on their point of origin. Thus we have cranial neural crest cells, vagal, trunk and lumbo-sacral (Fig. 1) (Le Douarin et al., 1993). Each population has different potentials regarding their derivatives and target areas.
Protective role of DDAH2 (rs805304) gene polymorphism in patients with myocardial infarction
2014, Experimental and Molecular PathologyCitation Excerpt :The functional prediction software used here predicted that rs3131383 and rs805305 polymorphisms have a potential functional effect, and these variants produce binding sites for the transcriptional factors AP2, CDP, CP2, HAND1, PAX, and ZF. AP2, CDP, HAND1, and PAX have been shown to act both as a repressor and an activator for regulated gene expression, morphogenesis, and differentiation in a wide target genes (Le Douarin et al., 1993) and are involved in congenital heart disease (Reamon-Buettner et al., 2009), and have a role in cell cycle progression (Gupta et al., 2003). CP2 acts as an oncogene in hepatocellular carcinoma and has a role in chemoresistance (Yoo et al., 2010).
The Spheno-occipital synchondrosis fuses prematurely in patients with crouzon syndrome and midface hypoplasia compared with age- and gender-matched controls
2014, Journal of Oral and Maxillofacial SurgeryCitation Excerpt :Because midface hypoplasia is typically more marked in patients with Crouzon and Apert syndrome than in those with Muenke syndrome, the results of our study and those of previous studies11,15-17 suggest a direct correlation between the age of fusion and the degree of midface hypoplasia in these patient populations. The cranial base plays an important role in craniofacial development,13,14,18,19 with the anterior cranial base considered a primary driver of midfacial growth.20,21 Synchondroses form between prominent ossification centers during cranial base development.
A homozygous missense variant in the PLCB4 gene causes severe phenotype of auriculocondylar syndrome type 2
2023, American Journal of Medical Genetics, Part A