May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
FGF Signaling Controls the Retinal Fissure Closure by Orchestrating Proliferation, Cell Fate Switches and Morphological Changes
Author Affiliations & Notes
  • S. Chen
    Stowers Institute Medical Res, Kansas City, Missouri
    Xie Lab,
  • T. Johnson
    Stowers Institute Medical Res, Kansas City, Missouri
  • R. McKay
    Stowers Institute Medical Res, Kansas City, Missouri
  • C. Deng
    Genetics of Development and Disease Branch, NIDDK, NIH, Bethesda, Maryland
  • Y. Furuta
    Department of Biochemistry and Molecular Biology, University of Texas, M.D. Anderson Cancer Center, Houston, Texas
  • N. Zhang
    Stowers Institute Medical Res, Kansas City, Missouri
  • T. Xie
    Stowers Institute Medical Res, Kansas City, Missouri
  • Footnotes
    Commercial Relationships  S. Chen, None; T. Johnson, None; R. McKay, None; C. Deng, None; Y. Furuta, None; N. Zhang, None; T. Xie, None.
  • Footnotes
    Support  Stowers Institute for Medical Research
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 1319. doi:https://doi.org/
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    • Get Citation

      S. Chen, T. Johnson, R. McKay, C. Deng, Y. Furuta, N. Zhang, T. Xie; FGF Signaling Controls the Retinal Fissure Closure by Orchestrating Proliferation, Cell Fate Switches and Morphological Changes. Invest. Ophthalmol. Vis. Sci. 2008;49(13):1319. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : Coloboma is a congenital disease, which is caused by the failure in closing the optic fissure (OF), a transient opening on the ventral side of the developing eye. Although mutations in several genes are known to cause coloboma, the cellular mechanisms underlying coloboma formation remain obscure. In this study, we use Fgfr conditional knockout mouse eyes as model to study the molecular and cellular mechanisms underlining the coloboma formation.

Methods: : We used Cre-LoxP system to conditionally knockout Fgfr1 and Fgfr2 from developing mouse eye. E10.5 to E12 embryonic eyes are subjected to immunohistochemistry, in situ hybridization and microarray analysis to reveal the cellular and molecular mechanisms that lead to coloboma phenotype developed in Fgfr mutant eyes.

Results: : . Conditional knockout of Fgfr1 and Fgfr2 function specifically from the optic cup causes the formation of coloboma. We also have observed the retarded retinal cell proliferation, an error in cell fate switch of OF progenitor cells and failures in cell shape changes in Fgfr mutant eyes.

Conclusions: : Our results indicate that retinal cell proliferation, cell fate switches and dynamic changes in cell shapes appear to drive the OF closure, and FGF signaling is involved in controlling the OF closing process by orchestrating these events. The celluar mechanisms contributing to coloboma formation revealed in mice will be useful for understanding how coloboma develops in humans

Keywords: retina • development • optic disc 
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