scholarly journals Rbms3 functions in craniofacial development by posttranscriptionally modulating TGF-β signaling

2012 ◽  
Vol 199 (3) ◽  
pp. 453-466 ◽  
Author(s):  
Chathurani S. Jayasena ◽  
Marianne E. Bronner
Keyword(s):  
Neural Crest ◽  
Rna Binding ◽  
Transforming Growth Factor ◽  
Neural Crest Cells ◽  
Transforming Growth Factor Β ◽  
Facial Skeleton ◽  
Altered Expression ◽  
Rna Immunoprecipitation ◽  
Β Receptor ◽  
Cranial Neural Crest Cells

Cranial neural crest cells form much of the facial skeleton, and abnormalities in their development lead to severe birth defects. In a novel zebrafish protein trap screen, we identified an RNA-binding protein, Rbms3, that is transiently expressed in the cytoplasm of condensing neural crest cells within the pharyngeal arches. Morphants for rbms3 displayed reduced proliferation of prechondrogenic crest and significantly altered expression for chondrogenic/osteogenic lineage markers. This phenotype strongly resembles cartilage/crest defects observed in Tgf-βr2:Wnt1-Cre mutants, which suggests a possible link with TGF-β signaling. Consistent with this are the findings that: (a) Rbms3 stabilized a reporter transcript with smad2 3′ untranslated region, (b) RNA immunoprecipitation with full-length Rbms3 showed enrichment for smad2/3, and (c) pSmad2 levels were reduced in rbms3 morphants. Overall, these results suggest that Rbms3 posttranscriptionally regulates one of the major pathways that promotes chondrogenesis, the transforming growth factor β receptor (TGF-βr) pathway.

TGF-β Signaling and its Functional Significance in Regulating the Fate of Cranial Neural Crest Cells

2003 ◽  
Vol 14 (2) ◽  
pp. 78-88 ◽  
Author(s):  
Y. Chai ◽  
Y. Ito ◽  
J. Han
Keyword(s):  
Neural Crest ◽  
Transforming Growth Factor ◽  
Neural Crest Cells ◽  
Transforming Growth Factor Β ◽  
Cell Types ◽  
Cranial Neural Crest ◽  
Multipotent Progenitors ◽  
Smad Proteins ◽  
Β Receptor ◽  
Cranial Neural Crest Cells

Members of the transforming growth factor-β (TGF-β) superfamily regulate cell proliferation, differentiation, and apoptosis, and control the development and maintenance of most tissues. TGF-β signal is transmitted through the phosphorylation of Smad proteins by TGF-β receptor serine/threonine kinase. During craniofacial development, TGF-β may regulate the fate specification of cranial neural crest cells. These cells are multipotent progenitors and capable of producing diverse cell types upon differentiation. Here we summarize evidence that TGF-β ligands and their signaling intermediates have significant roles in patterning and specification of cranial neural crest cells. The biological function of TGF-β is carried out through the regulation of transcriptional factors during embryogenesis.

scholarly journals A novel spalt gene expressed in branchial arches affects the ability of cranial neural crest cells to populate sensory ganglia

2004 ◽  
Vol 1 (1) ◽  
pp. 57-63 ◽  
Author(s):  
MEYER BAREMBAUM ◽  
MARIANNE BRONNER-FRASER
Keyword(s):  
Neural Crest ◽  
Trigeminal Ganglion ◽  
Neural Tube ◽  
Cell Lineage ◽  
Neural Crest Cells ◽  
Cranial Neural Crest ◽  
Facial Skeleton ◽  
Differentiation Markers ◽  
Branchial Arches ◽  
Cranial Neural Crest Cells

Cranial neural crest cells differentiate into diverse derivatives including neurons and glia of the cranial ganglia, and cartilage and bone of the facial skeleton. Here, we explore the function of a novel transcription factor of the spalt family that might be involved in early cell-lineage decisions of the avian neural crest. The chicken spalt4 gene (csal4) is expressed in the neural tube, migrating neural crest, branchial arches and, transiently, in the cranial ectoderm. Later, it is expressed in the mesectodermal, but not neuronal or glial, derivatives of midbrain and hindbrain neural crest. After over-expression by electroporation into the cranial neural tube and neural crest, we observed a marked redistribution of electroporated neural crest cells in the vicinity of the trigeminal ganglion. In control-electroporated embryos, numerous, labeled neural crest cells (∼80% of the population) entered the ganglion, many of which differentiated into neurons. By contrast, few (∼30% of the population) spalt-electroporated neural crest cells entered the trigeminal ganglion. Instead, they localized in the mesenchyme around the ganglionic periphery or continued further ventrally to the branchial arches. Interestingly, little or no expression of differentiation markers for neurons or other cell types was observed in spalt-electroporated neural crest cells.

scholarly journals Kat2a and Kat2b Acetyltransferase Activity Regulates Craniofacial Cartilage and Bone Differentiation in Zebrafish and Mice

2018 ◽  
Vol 6 (4) ◽  
pp. 27 ◽  
Author(s):  
Rwik Sen ◽  
Sofia Pezoa ◽  
Lomeli Carpio Shull ◽  
Laura Hernandez-Lagunas ◽  
Lee Niswander ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Cellular Growth ◽  
Cranial Neural Crest ◽  
Craniofacial Skeleton ◽  
Altered Expression ◽  
Precise Control ◽  
H3k9 Acetylation ◽  
Cranial Neural Crest Cells ◽  
And Cartilage

Cranial neural crest cells undergo cellular growth, patterning, and differentiation within the branchial arches to form cartilage and bone, resulting in a precise pattern of skeletal elements forming the craniofacial skeleton. However, it is unclear how cranial neural crest cells are regulated to give rise to the different shapes and sizes of the bone and cartilage. Epigenetic regulators are good candidates to be involved in this regulation, since they can exert both broad as well as precise control on pattern formation. Here, we investigated the role of the histone acetyltransferases Kat2a and Kat2b in craniofacial development using TALEN/CRISPR/Cas9 mutagenesis in zebrafish and the Kat2ahat/hat (also called Gcn5) allele in mice. kat2a and kat2b are broadly expressed during embryogenesis within the central nervous system and craniofacial region. Single and double kat2a and kat2b zebrafish mutants have an overall shortening and hypoplastic nature of the cartilage elements and disruption of the posterior ceratobranchial cartilages, likely due to smaller domains of expression of both cartilage- and bone-specific markers, including sox9a and col2a1, and runx2a and runx2b, respectively. Similarly, in mice we observe defects in the craniofacial skeleton, including hypoplastic bone and cartilage and altered expression of Runx2 and cartilage markers (Sox9, Col2a1). In addition, we determined that following the loss of Kat2a activity, overall histone 3 lysine 9 (H3K9) acetylation, the main epigenetic target of Kat2a/Kat2b, was decreased. These results suggest that Kat2a and Kat2b are required for growth and differentiation of craniofacial cartilage and bone in both zebrafish and mice by regulating H3K9 acetylation.

scholarly journals Neural crest cells require Meis2 for patterning the mandibular arch via the Sonic hedgehog pathway

Biology Open ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. bio052043
Author(s):  
Jaroslav Fabik ◽  
Katarina Kovacova ◽  
Zbynek Kozmik ◽  
Ondrej Machon
Keyword(s):  
Neural Crest ◽  
Sonic Hedgehog ◽  
Neural Crest Cells ◽  
Ectopic Ossification ◽  
Pharyngeal Arches ◽  
Altered Expression ◽  
Neural Crest Origin ◽  
Cranial Neural Crest Cells ◽  
Craniofacial Defects ◽  
Molecular Signals

ABSTRACTCranial neural crest cells (cNCCs) originate in the anterior neural tube and populate pharyngeal arches in which they contribute to formation of bone and cartilage. This cell population also provides molecular signals for the development of tissues of non-neural crest origin, such as the tongue muscles, teeth enamel or gland epithelium. Here we show that the transcription factor Meis2 is expressed in the oral region of the first pharyngeal arch (PA1) and later in the tongue primordium. Conditional inactivation of Meis2 in cNCCs resulted in loss of Sonic hedgehog signalling in the oropharyngeal epithelium and impaired patterning of PA1 along the lateral–medial and oral–aboral axis. Failure of molecular specification of PA1, illustrated by altered expression of Hand1/2, Dlx5, Barx1, Gsc and other markers, led to hypoplastic tongue and ectopic ossification of the mandible. Meis2-mutant mice thus display craniofacial defects that are reminiscent of several human syndromes and patients with mutations in the Meis2 gene.

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