A conserved role for non-neural ectoderm cells in early neural development

Cajal, Marieke; Creuzet, Sophie; Papanayotou, Costis; Sabéran‐Djoneidi, Délara; Lopes, Susana M. Chuva de Sousa; Zwijsen, An; Collignon, Jérôme; Camus, Anne

doi:10.1242/dev.107425

Cited by 14 publications

(13 citation statements)

References 79 publications

(74 reference statements)

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“…5C,G-I). Consistent with previous reports (Cajal et al, 2014;Camus et al, 2000;ElAmraoui and Dubois, 1993), ablations at neurula stages (HH7/8) caused a stronger phenotype: the AHP was largely absent or formed only by a few Lim3-positive cells (5/5; Fig. 5C,J-L), and did not undergo the thickening and invagination observed in control embryos (5/5; Fig.…”

Section: Median Ppe Cells Begin To Acquire An Ahp Character At the Nesupporting

confidence: 92%

Adenohypophysis placodal precursors exhibit distinctive features within the rostral preplacodal ectoderm

et al. 2017

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Placodes are discrete thickenings of the vertebrate cranial ectoderm that generate morpho-functionally distinct structures, such as the adenohypophysis, olfactory epithelium and lens. All placodes arise from a horseshoe-shaped preplacodal ectoderm in which the precursors of individual placodes are intermingled. However, fate-map studies indicated that cells positioned at the preplacodal midline give rise to only the adenohypophyseal placode, suggesting a unique organization of these precursors within the preplacode. To test this possibility, we combined embryological and molecular approaches in chick embryos to show that, at gastrula stage, adenohypophyseal precursors are clustered in the median preplacodal ectoderm, largely segregated from those of the adjacent olfactory placode. Median precursors are elongated, densely packed and, at neurula stage, express a molecular signature that distinguishes them from the remaining preplacodal cells. Olfactory placode precursors and midline neural cells can replace ablated adenohypophyseal precursors up to head-fold stage, although with a more plastic organization. We thus propose that adenohypophyseal placode precursors are unique within the preplacodal ectoderm possibly because they originate the only single placode and the only one with an endocrine character.

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Section: Median Ppe Cells Begin To Acquire An Ahp Character At the Nesupporting

confidence: 92%

Adenohypophysis placodal precursors exhibit distinctive features within the rostral preplacodal ectoderm

et al. 2017

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“…Second, it is possible that changes in NCC-derived facial mesenchyme induce changes in the neuroectoderm and FEZ that then contribute to the ciliary midfacial phenotype. There is precedence for NCCs exerting a critical effect on the developing forebrain [58–61], and we have previously observed aberrant morphology in the neuroectoderm of Kif3a fl/fl ;Wnt1-Cre mutant embryos [7]; however, how those dysmorphologies arise is unknown. Exploring if the establishment and/or maintenance of SHH signaling centers in the brain and face are disrupted in ciliary mutants is a focus of our ongoing work.…”

Section: Discussionmentioning

confidence: 99%

Craniofacial Ciliopathies Reveal Specific Requirements for GLI Proteins during Development of the Facial Midline

Chang

Millington

et al. 2016

PLoS Genet

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Ciliopathies represent a broad class of disorders that affect multiple organ systems. The craniofacial complex is among those most severely affected when primary cilia are not functional. We previously reported that loss of primary cilia on cranial neural crest cells, via a conditional knockout of the intraflagellar transport protein KIF3a, resulted in midfacial widening due to a gain of Hedgehog (HH) activity. Here, we examine the molecular mechanism of how a loss of primary cilia can produce facial phenotypes associated with a gain of HH function. We show that loss of intraflagellar transport proteins (KIF3a or IFT88) caused aberrant GLI processing such that the amount of GLI3FL and GLI2FL was increased, thus skewing the ratio of GLIFL to GLIR in favor of the FL isoform. Genetic addition of GLI3R partially rescued the ciliopathic midfacial widening. Interestingly, despite several previous studies suggesting midfacial development relies heavily on GLI3R activity, the conditional loss of GLI3 alone did not reproduce the ciliopathic phenotype. Only the combined loss of both GLI2 and GLI3 was able to phenocopy the ciliopathic midfacial appearance. Our findings suggest that ciliopathic facial phenotypes are generated via loss of both GLI3R and GLI2R and that this pathology occurs via a de-repression mechanism. Furthermore, these studies suggest a novel role for GLI2R in craniofacial development.

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“…The BMP and FGF pathways constantly seem to be intermingled in many developmental processes including neural induction (Cajal et al, 2014; Ishimura et al, 2000), mesoderm induction (S. Y. Lee et al, 2011; Northrop et al, 1995), and NC induction (Garnett, Square, & Medeiros, 2012; Yardley & Garcia-Castro, 2012).…”

Section: | Signaling Events Regulating Nc Inductionmentioning

confidence: 99%

Specifying neural crest cells: From chromatin to morphogens and factors in between

Rogers

Nie

2018

WIREs Developmental Biology

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Neural crest (NC) cells are a stem-like multipotent population of progenitor cells that are present in vertebrate embryos, traveling to various regions in the developing organism. Known as the "fourth germ layer", these cells originate in the ectoderm between the neural plate (NP), which will become the brain and spinal cord, and nonneural tissues that will become the skin and the sensory organs. NC cells can differentiate into more than 30 different derivatives in response to the appropriate signals including, but not limited to, craniofacial bone and cartilage, sensory nerves and ganglia, pigment cells, and connective tissue. The molecular and cellular mechanisms that control the induction and specification of NC cells include epigenetic control, multiple interactive and redundant transcriptional pathways, secreted signaling molecules, and adhesion molecules. NC cells are important not only because they transform into a wide variety of tissue types, but also because their ability to detach from their epithelial neighbors and migrate throughout developing embryos utilizes mechanisms similar to those used by metastatic cancer cells. In this review, we discuss the mechanisms required for the induction and specification of NC cells in various vertebrate species, focusing on the roles of early morphogenesis, cell adhesion, signaling from adjacent tissues, and the massive transcriptional network that controls the formation of these amazing cells. This article is categorized under: Nervous System Development > Vertebrates: General Principles Gene Expression and Transcriptional Hierarchies > Regulatory Mechanisms Gene Expression and Transcriptional Hierarchies > Gene Networks and Genomics Signaling Pathways > Cell Fate Signaling.

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A conserved role for non-neural ectoderm cells in early neural development

Cited by 14 publications

References 79 publications

Adenohypophysis placodal precursors exhibit distinctive features within the rostral preplacodal ectoderm

Adenohypophysis placodal precursors exhibit distinctive features within the rostral preplacodal ectoderm

Craniofacial Ciliopathies Reveal Specific Requirements for GLI Proteins during Development of the Facial Midline

Specifying neural crest cells: From chromatin to morphogens and factors in between

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