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FGF and Notch signaling hierarchy in sensory neurogenesis (651.18)
Author(s) -
Voelkel Jacob,
Harvey Jamison,
Adams Jason,
Lassiter Rhonda,
Stark Michael,
Molteni Agostino
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.651.18
Subject(s) - notch signaling pathway , neurogenesis , downregulation and upregulation , fibroblast growth factor , microbiology and biotechnology , proneural genes , trigeminal ganglion , biology , fgf and mesoderm formation , notch 1 , medicine , endocrinology , chemistry , signal transduction , neuroscience , sensory system , receptor , embryo , stem cell , progenitor cell , embryogenesis , biochemistry , ectoderm , gene
The purpose of this study was to determine the regulatory relationship of sensory neurogenesis in the trigeminal placode between the Fibroblast Growth Factor (FGF) and Notch signaling pathways. To do this, FGF signaling was blocked cell autonomously or globally while simultaneously downregulating Notch signaling in 10‐12 somite stage Gallus gallus chick embryos. Cell autonomous FGF inhibition with global Notch downregulation significantly reduced the number of proneural cells contributing the future trigeminal ganglion (p=0.0002). A similar reduction was found with concurrent global inhibition of FGF and Notch (p<0.0001). Remarkably, blocking FGF either cell autonomously or globally with simultaneous Notch downregulation reversed the effects of robust neurogenesis seen with Notch downregulation alone (p<0.0001). Further, Notch downregulation for 4 or 12 hours showed no difference in the level of FGF‐receptor 4 mRNA expression when compared to controls. It did however result in a highly fragmented basal lamina, which was reversed when blocking FGF signaling. From these data, we invalidate the FGF downregulates Notch in sensory neurogenesis model and propose a mechanism for parallel regulation of FGF and Notch leading to basement membrane fragmentation and subsequent delamination of differentiating opV placode cells. Grant Funding Source : Supported by NIH/NICHD ‐ R01 HD046475