
FGF signaling is critical in the development of the vertebrate retina, which differentiates in a wave-like pattern similar to that found in theDrosophilaeye. In this study, we investigated the mechanism of FGF signaling in vertebrate eye development by identifying Shp2, a protein tyrosine phosphatase, as a novel factor in orchestrating retinal morphogenesis. Using a series ofShp2conditional mutants, we have shown thatShp2is specifically required for the initiation of retinal neurogenesis but not for the maintenance of the retinal differentiation program. By mosaic deletion ofShp2, we further demonstrated thatShp2ablation did not prevent the spreading of the retinal differentiation wave. Shp2 instead controls the patterning of the optic vesicle by regulating the retinal progenitor factors and cell proliferation. Inex vivoculture models and genetic rescue experiments, we showed thatShp2acts downstream to FGF signaling in retinal development and that it can be functionally substituted by activated Ras signaling. Together, these results demonstrate that Shp2 mediates FGF–Ras signaling to control retinal progenitor cell fate.
Neurons, Time Factors, Neurogenesis, Age Factors, Cell Differentiation, Mice, Transgenic, Protein Tyrosine Phosphatase, Non-Receptor Type 11, Retina, Fibroblast Growth Factors, Mice, Organ Culture Techniques, Paracrine Communication, Animals, Gene Deletion
Neurons, Time Factors, Neurogenesis, Age Factors, Cell Differentiation, Mice, Transgenic, Protein Tyrosine Phosphatase, Non-Receptor Type 11, Retina, Fibroblast Growth Factors, Mice, Organ Culture Techniques, Paracrine Communication, Animals, Gene Deletion
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