A vertebrate crossveinless 2 homologue modulates BMP activity and neural crest cell migration

Coles, Edward G.; Christiansen, Jeffrey H.; Economou, Androulla; Bronner‐Fraser, Marianne; Wilkinson, David G.

doi:10.1242/dev.01419

Cited by 59 publications

(57 citation statements)

References 38 publications

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“…Noggin overexpression inhibits BMP4 and Wnt1 expression, whereas in embryos grafted with Noggin-producing cells, -catenin overexpression rescues delamination and reactivates G1/S transition in the neural crest (Burstyn-Cohen et al, 2004). BMP is modulated by crossveinless 2 (Cv-2), which causes premature neural crest migration when overexpressed (Coles et al, 2004). BMP-Wnt signaling is also triggered by retinoid acid (RA), which forms a rostrocaudal gradient in the paraxial mesoderm.…”

Section: Delamination and Emtmentioning

confidence: 99%

Epithelial-mesenchymal transitions: insights from development

2012

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Epithelial-mesenchymal transition (EMT) is a crucial, evolutionarily conserved process that occurs during development and is essential for shaping embryos. Also implicated in cancer, this morphological transition is executed through multiple mechanisms in different contexts, and studies suggest that the molecular programs governing EMT, albeit still enigmatic, are embedded within developmental programs that regulate specification and differentiation. As we review here, knowledge garnered from studies of EMT during gastrulation, neural crest delamination and heart formation have furthered our understanding of tumor progression and metastasis.Key words: Epithelial-mesenchymal transition, Gastrulation, Neural crest, Heart morphogenesis Introduction Epithelial-mesenchymal transition (EMT) is an evolutionarily conserved developmental process that contributes to the formation of the body plan, histogenesis and organogenesis. In the late 19th century, mesenchymal and epithelial cells were recognized as having distinct phenotypes (Duval, 1879) and, although EMT was apparent to embryologists (Platt, 1894), it only became interesting to developmental biologists in the 1960s. Following pioneering work from Elizabeth Hay (Greenburg and Hay, 1982; Hay, 2005), we now know that epithelial cells lose apicobasal polarity and intercellular junctions during EMT. These changes in cell polarity and adhesion disrupt the epithelial basement membrane and allow cellular penetration into an extracellular matrix (ECM)-rich compartment: a process referred to as delamination (see Glossary, Box 1). These newly formed mesenchymal cells transiently express distinct mesenchymal markers, acquire a front-rear polarity and become invasive, favoring cell-ECM rather than cell-cell adhesions.Interestingly, EMT is not irreversible: cells frequently cycle between epithelial and mesenchymal states via EMT and the reverse process, mesenchymal-epithelial transition (MET). Importantly, EMT has been implicated in pathological conditions, such as organ fibrosis, and in cancer, where it contributes to tumor progression and metastasis (Kalluri and Weinberg, 2009;Thiery et al., 2009). As such, much effort has been devoted to understanding the molecular regulation of EMT during development as an insight into the role and regulation of EMT in pathology.EMT is context dependent, occurring within the framework of other signaling mechanisms, such as cell fate induction, commitment and differentiation. However, the precise events that drive EMT are not fully understood. Genetic studies in Drosophila originally identified the transcription factors Twist and Snail as potential drivers of EMT during gastrulation (Leptin and Grunewald, 1990). Soon after, a Snail ortholog, Slug (Snai2), was shown to be involved in EMT in chicken embryo gastrulation (Nieto et al., 1994). Since then, several genes encoding transcription factors, cell polarity proteins and effector proteins have been shown to govern EMT in normal and transformed epithelial cells (see Table 1), suggesting tha...

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Section: Delamination and Emtmentioning

confidence: 99%

Epithelial-mesenchymal transitions: insights from development

2012

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“…But Cv2 proteins are not simple co-receptors, as they can also inhibit signaling. Cv2 regulates BMP signaling in early axis formation in Xenopus (Ambrosio et al, 2008), as well as axis formation, hematopoiesis and vascular development in zebrafish (Moser et al, 2007;Rentzsch et al, 2006), neural crest formation in chick (Coles et al, 2004) and skeletogenesis in mice (Ikeya et al, 2006;Ikeya et al, 2008;Zakin et al, 2008). But the direction of that modulation varies, even in contexts that appear homologous (e.g.…”

Section: Context-dependent Effects On Bmp Signal Reception: Crossveinmentioning

confidence: 99%

The extracellular regulation of bone morphogenetic protein signaling

2009

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In many cases, the level, positioning and timing of signaling through the bone morphogenetic protein (BMP) pathway are regulated by molecules that bind BMP ligands in the extracellular space. Whereas many BMP-binding proteins inhibit signaling by sequestering BMPs from their receptors, other BMP-binding proteins cause remarkably context-specific gains or losses in signaling. Here, we review recent findings and hypotheses on the complex mechanisms that lead to these effects, with data from developing systems, biochemical analyses and mathematical modeling.

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“…Much effort has been expended interrogating the gene regulatory networks underlying NC development (Sauka-Spengler and Bronner-Fraser, 2008). Major signaling pathways, including Wnt, Fgf, Bmp and Notch signaling, have been shown to play important roles in regulating NC induction, proliferation and migration (Sela-Donenfeld and Kalcheim, 1999;Garcia-Castro et al, 2002;Coles et al, 2004;Glavic et al, 2004;Carmona-Fontaine et al, 2008). However, the function of Hippo signaling in CNC development remains poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Yap and Taz play a crucial role in neural crest-derived craniofacial development

et al. 2015

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The role of the Hippo signaling pathway in cranial neural crest (CNC) development is poorly understood. We used the Wnt1Cre and Wnt1Cre2SOR drivers to conditionally ablate both Yap and Taz in the CNC of mice. When using either Cre driver, Yap and Taz deficiency in the CNC resulted in enlarged, hemorrhaging branchial arch blood vessels and hydrocephalus. However, Wnt1Cre2SOR embryos had an open cranial neural tube phenotype that was not evident in Wnt1Cre embryos. In O9-1 CNC cells, the loss of Yap and Taz impaired smooth muscle cell differentiation. RNA-sequencing data indicated that Yap and Taz regulate genes encoding Fox transcription factors, specifically Foxc1. Proliferation was reduced in the branchial arch mesenchyme of Yap and Taz CNC conditional knockout (CKO) embryos. Moreover, Yap and Taz CKO embryos had cerebellar aplasia similar to Dandy Walker spectrum malformations observed in human patients and mouse embryos with mutations in Foxc1. In embryos and O9-1 cells deficient for Yap and Taz, Foxc1 expression was significantly reduced. Analysis of Foxc1 regulatory regions revealed a conserved recognition element for the Yap and Taz DNA binding co-factor Tead. ChIP-pcr experiments further supported the conclusion that Foxc1 is directly regulated by the Yap/Tead complex. Our findings uncover important roles for Yap and Taz in CNC diversification and development.

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A vertebrate crossveinless 2 homologue modulates BMP activity and neural crest cell migration

Cited by 59 publications

References 38 publications

Epithelial-mesenchymal transitions: insights from development

Epithelial-mesenchymal transitions: insights from development

The extracellular regulation of bone morphogenetic protein signaling

Yap and Taz play a crucial role in neural crest-derived craniofacial development

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