May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Shp2 Regulates Ras-Erk Signaling in Lens and Lacrimal Gland Development
Author Affiliations & Notes
  • X. Zhang
    Medical & Molecular Genetics, Indiana Univ Sch of Medicine, Indianapolis, Indiana
  • Y. Pan
    Medical & Molecular Genetics, Indiana Univ Sch of Medicine, Indianapolis, Indiana
  • A. Powers
    Medical & Molecular Genetics, Indiana Univ Sch of Medicine, Indianapolis, Indiana
  • G.-S. Feng
    Programs in Signal Transduction and Stem Cells & Regeneration, Burnham Institute for Medical Research, La Jolla, California
  • Footnotes
    Commercial Relationships  X. Zhang, None; Y. Pan, None; A. Powers, None; G. Feng, None.
  • Footnotes
    Support  NIH (EY017061 to XZ, CA78606 to GSF)
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 1139. doi:https://doi.org/
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      X. Zhang, Y. Pan, A. Powers, G.-S. Feng; Shp2 Regulates Ras-Erk Signaling in Lens and Lacrimal Gland Development. Invest. Ophthalmol. Vis. Sci. 2008;49(13):1139. doi: https://doi.org/.

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

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Abstract

Purpose: : Previous studies have identified protein tyrosine phosphatase Shp2 as an important regulator of receptor tyrosine kinase (RTK) signaling, including FGF signal transduction. Moreover, when a Shp2 interaction site was mutated in FRS2α, an intracellular mediator of FGF signaling, it disrupted the lens development in mouse. We therefore investigated the functional requirement of Shp2 in eye development.

Methods: : The Shp2 lens and lacrimal gland specific knockout mutants are analyzed by RNA in situ hybridization and immunohistochemistry.

Results: : We demonstrate that inactivation of Shp2 disrupts both lens and lacrimal gland development. Although crystallin expression is still present, the Shp2 mutant lens exhibits delayed lens cell differentiation, increasing cell apoptosis and reduced cell proliferation. In addition, lacrimal gland budding is completely abolished in the Shp2 mutants. Consistent with disruption of ERK signaling, expressions of phospho-ERK and ERM are also down-regulated. Finally, we show that Shp2 genetically interacts with Ras signaling in eye development.

Conclusions: : These results establish an important role of Shp2 in lens and lacrimal gland development.

Keywords: development • signal transduction • lacrimal gland 
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