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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.
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© ARVO (1962-2015); The Authors (2016-present)
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.
The Shp2 lens and lacrimal gland specific knockout mutants are analyzed by RNA in situ hybridization and immunohistochemistry.
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.
These results establish an important role of Shp2 in lens and lacrimal gland development.
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