PUBLICATION

Rbms3 functions in craniofacial development by posttranscriptionally modulating TGF-? signaling

Authors
Jayasena, C.S., and Bronner, M.E.
ID
ZDB-PUB-121102-28
Date
2012
Source
The Journal of cell biology   199(3): 453-466 (Journal)
Registered Authors
Bronner-Fraser, Marianne, Jayasena, Chathurani (Saku)
Keywords
none
MeSH Terms
  • Apoptosis
  • Chondrogenesis/physiology*
  • Cell Differentiation
  • Immunoprecipitation
  • Zebrafish/embryology
  • Zebrafish/metabolism*
  • Blotting, Western
  • Craniofacial Abnormalities/genetics
  • Craniofacial Abnormalities/metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • RNA Processing, Post-Transcriptional*
  • Receptors, Transforming Growth Factor beta/genetics
  • Receptors, Transforming Growth Factor beta/metabolism
  • Real-Time Polymerase Chain Reaction
  • Amino Acid Sequence
  • Cartilage/cytology
  • Cartilage/metabolism
  • Neural Crest/cytology
  • Neural Crest/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
  • In Situ Hybridization
  • RNA-Binding Proteins/genetics
  • RNA-Binding Proteins/metabolism
  • Cell Proliferation
  • Gene Expression Regulation, Developmental
  • Transforming Growth Factor beta/genetics*
  • Transforming Growth Factor beta/metabolism
  • Fluorescent Antibody Technique
  • Molecular Sequence Data
  • Signal Transduction
  • RNA, Messenger/genetics
  • Animals
  • Embryo, Nonmammalian/cytology
  • Embryo, Nonmammalian/metabolism
PubMed
23091072 Full text @ J. Cell Biol.
Abstract

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 32 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.

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