Cell Fate Decisions in a Human Retinal Precursor Cell Line: Basic Fibroblast Growth Factor- and Transforming Growth Factor-α-Mediated Differentiation

2000 ◽  
Vol 19 (9) ◽  
pp. 527-537 ◽  
Author(s):  
Ifeoma Ezeonu ◽  
Bryan Derrickson ◽  
Kamla Dutt
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cell Fate ◽  
Transforming Growth Factor ◽  
Precursor Cell ◽  
Fibroblast Growth ◽  
Transforming Growth Factor Α ◽  
Cell Fate Decisions ◽  
Precursor Cell Line ◽  
Factor Α

A role for the fibroblast growth factor receptor in cell fate decisions in the developing vertebrate retina

Development ◽  
1998 ◽  
Vol 125 (20) ◽  
pp. 3967-3975 ◽  
Author(s):  
S. McFarlane ◽  
M.E. Zuber ◽  
C.E. Holt
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cell Fate ◽  
Fibroblast Growth Factor Receptor ◽  
Growth Factor Receptor ◽  
Retinal Cell ◽  
Fibroblast Growth ◽  
Cell Fate Decisions ◽  
Mutant Receptor ◽  
Vertebrate Retina

The mature vertebrate retina contains seven major cell types that develop from an apparently homogenous population of precursor cells. Clonal analyses have suggested that environmental influences play a major role in specifying retinal cell identity. Fibroblast growth factor-2 is present in the developing retina and regulates the survival, proliferation and differentiation of developing retinal cells in culture. Here we have tested whether fibroblast growth factor receptor signaling biases retinal cell fate decisions in vivo. Fibroblast growth factor receptors were inhibited in retinal precursors in Xenopus embryos by expressing a dominant negative form of the receptor, XFD. Dorsal animal blastomeres that give rise to the retina were injected with cDNA expression constructs for XFD and a control non-functional mutant receptor, D48, and the cell fates of transgene-expressing cells in the mature retina determined. Fibroblast growth factor receptor blockade results in almost a 50% loss of photoreceptors and amacrine cells, and a concurrent 3.5-fold increase in Muller glia, suggesting a shift towards a Muller cell fate in the absence of a fibroblast growth factor receptor signal. Inhibition of non-fibroblast-growth-factor-mediated receptor signaling with a third mutant receptor, HAVO, alters cell fate in an opposite manner. These results suggest that it is the balance of fibroblast growth factor and non-fibroblast growth factor ligand signals that influences retinal cell genesis.

Mouse Serrate-1 (Jagged-1): expression in the developing tooth is regulated by epithelial-mesenchymal interactions and fibroblast growth factor-4

Development ◽  
1997 ◽  
Vol 124 (8) ◽  
pp. 1473-1483 ◽  
Author(s):  
T.A. Mitsiadis ◽  
D. Henrique ◽  
I. Thesleff ◽  
U. Lendahl
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cell Fate ◽  
Tooth Development ◽  
Expression Patterns ◽  
Control Cell ◽  
Fibroblast Growth ◽  
Down Regulation ◽  
Cell Fate Decisions ◽  
Dental Epithelium

Serrate-like genes encode transmembrane ligands to Notch receptors and control cell fate decisions during development. In this report, we analyse the regulation of the mouse Serrate-1 gene during embryogenesis. The Serrate-1 gene is expressed from embryonic day 7.5 (E7.5) and expression is often observed at sites of epithelial-mesenchymal interactions, including the developing tooth, where Serrate-1 is first (E11.5) expressed in all cells of the dental epithelium, but not in mesenchyme. A transient upregulation in dental mesenchyme (E12.5-15.5) is correlated with down-regulation of Serrate-1 expression in epithelial cells contacting the mesenchyme, i.e. in the cells destined to become ameloblasts. This expression pattern is reproduced in explants of dental epithelium and mesenchyme in vitro: epithelium induces Serrate-1 expression in mesenchyme, while epithelium in close proximity to this mesenchyme does not express detectable levels of Serrate-1 mRNA, suggesting that down-regulation of Serrate-1 expression in preameloblasts is caused by mesenchyme-derived signals. Finally, regulation of Serrate-1 expression differs from that of Notch genes. The Serrate-1 gene is induced in dental mesenchyme by fibroblast growth factor-4, but not by bone morphogenetic proteins, while the converse is true for Notch genes. This indicates that, at least during tooth development, the expression patterns observed for receptors and ligands in the Notch signaling pathway are generated by different induction mechanisms.

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