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 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.

Laser capture microdissection of fluorescently labeled embryonic cranial neural crest cells

genesis ◽  
2004 ◽  
Vol 39 (1) ◽  
pp. 58-64 ◽  
Author(s):  
Vasker Bhattacherjee ◽  
Partha Mukhopadhyay ◽  
Saurabh Singh ◽  
Emily A. Roberts ◽  
Rita C. Hackmiller ◽  
...  
Keyword(s):  
Neural Crest ◽  
Laser Capture Microdissection ◽  
Neural Crest Cells ◽  
Cranial Neural Crest ◽  
Cranial Neural Crest Cells ◽  
Laser Capture

scholarly journals Transforming Growth Factor β-Mediated Transcriptional Repression of c-myc Is Dependent on Direct Binding of Smad3 to a Novel Repressive Smad Binding Element

2004 ◽  
Vol 24 (6) ◽  
pp. 2546-2559 ◽  
Author(s):  
Joshua P. Frederick ◽  
Nicole T. Liberati ◽  
David S. Waddell ◽  
Yigong Shi ◽  
Xiao-Fan Wang
Keyword(s):  
Growth Factor ◽  
Transcriptional Repression ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Cell Types ◽  
Specific Cell ◽  
Smad Proteins ◽  
Smad Binding Element

ABSTRACT Smad proteins are the most well-characterized intracellular effectors of the transforming growth factor β (TGF-β) signal. The ability of the Smads to act as transcriptional activators via TGF-β-induced recruitment to Smad binding elements (SBE) within the promoters of TGF-β target genes has been firmly established. However, the elucidation of the molecular mechanisms involved in TGF-β-mediated transcriptional repression are only recently being uncovered. The proto-oncogene c-myc is repressed by TGF-β, and this repression is required for the manifestation of the TGF-β cytostatic program in specific cell types. We have shown that Smad3 is required for both TGF-β-induced repression of c-myc and subsequent growth arrest in keratinocytes. The transcriptional repression of c-myc is dependent on direct Smad3 binding to a novel Smad binding site, termed a repressive Smad binding element (RSBE), within the TGF-β inhibitory element (TIE) of the c-myc promoter. The c-myc TIE is a composite element, comprised of an overlapping RSBE and a consensus E2F site, that is capable of binding at least Smad3, Smad4, E2F-4, and p107. The RSBE is distinct from the previously defined SBE and may partially dictate, in conjunction with the promoter context of the overlapping E2F site, whether the Smad3-containing complex actively represses, as opposed to transactivates, the c-myc promoter.

scholarly journals Cranial neural crest cells on the move: Their roles in craniofacial development

2010 ◽  
Vol 155 (2) ◽  
pp. 270-279 ◽  
Author(s):  
Dwight R. Cordero ◽  
Samantha Brugmann ◽  
Yvonne Chu ◽  
Ruchi Bajpai ◽  
Maryam Jame ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Craniofacial Development ◽  
Cranial Neural Crest ◽  
Cranial Neural Crest Cells
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