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1.  Rbms3 functions in craniofacial development by posttranscriptionally modulating TGF-β signaling 
The Journal of Cell Biology  2012;199(3):453-466.
Rbms3 regulates TGF-βr signaling, a critical pathway for chondrogenesis, by binding and stabilizing Smad2 transcripts.
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.
doi:10.1083/jcb.201204138
PMCID: PMC3483135  PMID: 23091072
2.  Live imaging of endogenous Collapsin response mediator protein-1 expression at subcellular resolution during zebrafish nervous system development 
Gene expression patterns : GEP  2011;11(7):395-400.
Collapsin response mediator proteins (CRMPs) are cytosolic phosphoproteins that are functionally important during vertebrate development. We have generated a zebrafish genetrap line that produces fluorescently tagged Crmp1 protein, which can be dynamically tracked in living fish at subcellular resolution. The results show that Crmp1 is expressed in numerous sites in the developing nervous system. Early expression is apparent in the forebrain, epiphysis, optic tectum and the developing spinal cord. In the larval brain, Crmp1 is expressed in several distinct brain regions, such as the telencephalon, habenula and cerebellum. In addition, it is expressed in the spinal cord in a manner that persists in the larva. The results suggest that this Crmp1 protein trap line offers a powerful tool to track selected neuronal populations at high resolution.
doi:10.1016/j.gep.2011.05.002
PMCID: PMC3163798  PMID: 21628002
Crmp1; zebrafish; nervous system; development
3.  Notch signaling augments the canonical Wnt pathway to specify the size of the otic placode 
Development (Cambridge, England)  2008;135(13):2251-2261.
SUMMARY
The inner ear derives from a patch of ectoderm defined by expression of the transcription factor Pax2. We recently showed this Pax2+ ectoderm gives rise not only to the otic placode but also to surrounding cranial epidermis, and that Wnt signaling mediates this placode-epidermis fate decision. We now present evidence for reciprocal interactions between the Wnt and Notch signaling pathways during inner ear induction. Activation of Notch1 in Pax2+ ectoderm expands the placodal epithelium at the expense of cranial epidermis, while loss of Notch1 leads to a reduction in the size of the otic placode. We show that Wnt signaling positively regulates Notch pathway genes such as Jag1, Notch1 and Hes1, and have used transgenic Wnt reporter mice to show that Notch signaling can modulate the canonical Wnt pathway. Gain and loss of function mutations in the Notch and Wnt pathways reveal that some aspects of otic placode development - such as Pax8 expression and the morphological thickening of the placode – can be regulated independently by either Notch or Wnt signals. Our results suggest that Wnt signaling specifies the size of the otic placode in two ways – by directly up-regulating a subset of otic genes, and by positively regulating components of the Notch signaling pathway which then act to augment Wnt signaling.
doi:10.1242/dev.017905
PMCID: PMC2575054  PMID: 18495817
Mouse; Otic placode; Wnt; β-catenin; Notch1; Jagged1; Inner ear

Results 1-3 (3)