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Z. Yu, J. Zhao, J. Zhang, Y.-H. Liu, S. Yiu, Y. Lallemand, V. Bensoussan, L. Zhu; Conditional Deletion of Msx2 in the Developing Lens Leads to Microphthalmia in Mice. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2349.
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© ARVO (1962-2015); The Authors (2016-present)
Msx form one of the most highly conserved families of homeobox-containing genes. Homeobox genes function as essential transcriptional regulators in a variety of developmental processes. Overexpression of the Msx2 gene in transgenic mice can alter Bmp4 and Bmp7 gene expression, initiate cellular apoptosis in the developing neural retina, and cause microphthalmia.In current experiments, we investigated the function of Msx2 in conditional knockout mice.
To learn more about the function of Msx2 during lens development, we examined mice in which the Msx2 was selectively deleted in the lens using Cre-IoxP-mediated gene targeting.
Msx2-defecient mice show a persistent lens stalk, a delay in lens formation and the micropthalmia at developmental stages. The delay in lens formation is associated with an increased apoptosis activity in the lens placode during its invagination into the optic cup. For lens lineage-specific transcriptional factors, the expression of FoxE3 is reduced but no obvious changes in Pax6, Sox2 and Ap2α expression are observed in the developing lens of Msx2-deficient mice compared to the wild-type littermates. The expression of FoxE3 in early eye development is under control of Msx2, and reduced expression involved in adherence between lens and cornea.
Our research results showed the Msx2 is critically required during the morphogenetic processes of early eye development.
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