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K. Sakagami, H. Wu, X.-J. Yang; Regulation of Cell Fate, Cell Migration, and Synaptogenesis by Pten in Mouse Retinal Development. Invest. Ophthalmol. Vis. Sci. 2009;50(13):1306.
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© ARVO (1962-2015); The Authors (2016-present)
The mature vertebrate neural retina consists of seven major types of neuronal and glial cells and is an excellent system for studying neuronal differentiation. Accumulating evidence indicates that development of neural retina is regulated by both cell-intrinsic factors and cell-extrinsic cues. Phosphatase with tensin homology (PTEN) was originally identified as a gene that is mutated in many types of tumors. PTEN is a lipid phosphatase and negatively regulates the phosphatidylinositol 3-kinase signaling (PI3K) pathway, especially in cells that are responding to growth factor stimulation. PTEN has also been shown to regulate cell proliferation, cell survival, and cell migration during central nervous system development. The purpose of this study is to elucidate the functions of PTEN and PI3K pathway during mouse retinal development.
We performed retina-specific ablation of PTEN gene using mice encoding PTEN floxed allele crossed with Chx10-Cre transgenic mice.
Cre/LoxP mediated deletion of PTEN in the retina results in an increased thickness of the neural retina with expanded synaptic layers. The mutant retinas also show displaced cells in the inner nuclear layer and inner plexiform layer, suggesting defects in cell migration. Quantifications of neuronal cell markers reveal altered production of retinal ganglion cell, amacrine cells, horizontal cells, photoreceptors, and Muller glia. Together, these results demonstrate the essential functions of PTEN in cell fate specification, cell migration, and synaptogenesis in the neural retina.
We propose that PTEN influences multiple aspects of mouse retinal development through negative modulation.
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