Relative expression of <i>Slug, RhoB,</i> and HNK‐1 in the cranial neural crest of the early chicken embryo

Barrio, Marta García del; Nieto, M. Ángela

doi:10.1002/dvdy.10456

Cited by 52 publications

(46 citation statements)

References 19 publications

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“…The onset of neural crest delamination varies considerably between the head and trunk of the vertebrate embryo (BurstynCohen et al, 2004;Del Barrio and Nieto, 2004;Theveneau et al, 2007). Snail2 (formally known as Slug) is expressed in cells undergoing EMT and in migrating CNC cells (Del Barrio and Nieto, 2004) (this study).…”

Section: Research Articlementioning

confidence: 81%

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p53 coordinates cranial neural crest cell growth and epithelial-mesenchymal transition/delamination processes

et al. 2011

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SUMMARYNeural crest development involves epithelial-mesenchymal transition (EMT), during which epithelial cells are converted into individual migratory cells. Notably, the same signaling pathways regulate EMT function during both development and tumor metastasis. p53 plays multiple roles in the prevention of tumor development; however, its precise roles during embryogenesis are less clear. We have investigated the role of p53 in early cranial neural crest (CNC) development in chick and mouse embryos. In the mouse, p53 knockout embryos displayed broad craniofacial defects in skeletal, neuronal and muscle tissues. In the chick, p53 is expressed in CNC progenitors and its expression decreases with their delamination from the neural tube. Stabilization of p53 protein using a pharmacological inhibitor of its negative regulator, MDM2, resulted in reduced SNAIL2 (SLUG) and ETS1 expression, fewer migrating CNC cells and in craniofacial defects. By contrast, electroporation of a dominant-negative p53 construct increased PAX7 + SOX9 + CNC progenitors and EMT/delamination of CNC from the neural tube, although the migration of these cells to the periphery was impaired. Investigating the underlying molecular mechanisms revealed that p53 coordinates CNC cell growth and EMT/delamination processes by affecting cell cycle gene expression and proliferation at discrete developmental stages; disruption of these processes can lead to craniofacial defects.

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Section: Research Articlementioning

confidence: 81%

“…Snail2 (formally known as Slug) is expressed in cells undergoing EMT and in migrating CNC cells (Del Barrio and Nieto, 2004) (this study). It was shown recently that Ets1, a protooncogene that is specifically expressed in CNC cells, works together with Snail2 to promote CNC delamination (Theveneau et al, 2007).…”

Section: Research Articlementioning

confidence: 95%

p53 coordinates cranial neural crest cell growth and epithelial-mesenchymal transition/delamination processes

et al. 2011

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“…After culture, we monitored the generation of neural, rostral placodal, neural crest and epidermal cells on consecutive sections of the explants. By stage 10, Sox1 is expressed exclusively in neural progenitor cells (Patthey et al, 2008;Wood and Episkopou, 1999), Snail2 (previously known as Slug) is preferentially expressed in premigratory and early migratory neural crest cells, HNK-1 is expressed in migratory neural crest (Del Barrio and Nieto, 2004), cytokeratins (Ker) and Sox2 are coexpressed in prospective cranial placodes, and Ker expression alone defines cells of epidermal character (Comte et al, 2004;Rex et al, 1997;Wood and Episkopou, 1999) (Fig. 1B) (Fig.…”

Section: Resultsmentioning

confidence: 99%

Wnt-regulated temporal control of BMP exposure directs the choice between neural plate border and epidermal fate

2009

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The non-neural ectoderm is divided into neural plate border and epidermal cells. At early blastula stages, Wnt and BMP signals interact to induce epidermal fate, but when and how cells initially acquire neural plate border fate remains poorly defined. We now provide evidence in chick that the specification of neural plate border cells is initiated at the late blastula stage and requires both Wnt and BMP signals. Our results indicate, however, that at this stage BMP signals can induce neural plate border cells only when Wnt activity is blocked, and that the two signals in combination generate epidermal cells. We also provide evidence that Wnt signals do not play an instructive role in the generation of neural plate border cells, but promote their generation by inducing BMP gene expression, which avoids early simultaneous exposure to the two signals and generates neural plate border instead of epidermal cells. Thus, specification of neural plate border cells is mediated by a novel Wnt-regulated BMP-mediated temporal patterning mechanism.

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“…1J) (Nieto et al, 1994;del Barrio and Nieto, 2004). Within the neural tube, all cells that expressed LSox5 also expressed Slug (Fig.…”

Section: Lsox5 Is Expressed In Premigratory and Migratory Cephalic Nementioning

confidence: 92%

LSox5 regulates RhoB expression in the neural tube and promotes generation of the neural crest

2004

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Members of the Sox family of transcription factors are involved in a number of crucial developmental processes, including sex determination, neurogenesis and skeletal development. LSox5 is a member of the group D Sox factors that,in conjunction with Sox6 and Sox9, promotes chondrogenesis by activating the expression of cartilage-specific extracellular matrix molecules. We have cloned the chicken homologue of LSox5 and found that it is initially expressed in the premigratory and migratory neural crest after Slugand FoxD3. Subsequently, the expression of LSox5 is maintained in cephalic crest derivatives, and it appears to be required for the development of the glial lineage, the Schwann cells and satellite glia in cranial ganglia. Misexpression of LSox5 in the cephalic neural tube activated RhoB expression throughout the dorsoventral axis. Furthermore, the prolonged forced expression of LSox5 enlarged the dorsal territory in which the neural crest is generated, extended the `temporal window' of neural crest segregation, and led to an overproduction of neural crest cells in cephalic regions. In addition to HNK-1, the additional neural crest cells expressed putative upstream markers (Slug, FoxD3) indicating that a regulatory feedback mechanism may operate during neural crest generation. Thus, our data show that in addition to the SoxE genes(Sox9 and Sox10) a SoxD gene (Sox5) also participates in neural crest development and that a cooperative interaction may operate during neural crest generation, as seen during the formation of cartilage.

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Relative expression of Slug, RhoB, and HNK‐1 in the cranial neural crest of the early chicken embryo

Cited by 52 publications

References 19 publications

p53 coordinates cranial neural crest cell growth and epithelial-mesenchymal transition/delamination processes

p53 coordinates cranial neural crest cell growth and epithelial-mesenchymal transition/delamination processes

Wnt-regulated temporal control of BMP exposure directs the choice between neural plate border and epidermal fate

LSox5 regulates RhoB expression in the neural tube and promotes generation of the neural crest

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