| First Author | Fu X | Year | 2006 |
| Journal | Dev Biol | Volume | 299 |
| Issue | 2 | Pages | 424-37 |
| PubMed ID | 16959241 | Mgi Jnum | J:115047 |
| Mgi Id | MGI:3690586 | Doi | 10.1016/j.ydbio.2006.08.015 |
| Citation | Fu X, et al. (2006) Beta-catenin is essential for lamination but not neurogenesis in mouse retinal development. Dev Biol 299(2):424-37 |
| abstractText | During vertebrate retinal development, the seven retinal cell types differentiate sequentially from a single population of retinal progenitor cells (RPCs) and organize themselves into a distinct laminar structure. The purpose of this study was to determine whether beta-catenin, which functions both as a nuclear effector for the canonical Wnt signaling pathway and as a regulator of cell adhesion, is required for retinal neurogenesis or lamination. We used the Cre-loxP system to either eliminate beta-catenin or to express a constitutively active form during retinal neurogenesis. Eliminating beta-catenin did not affect cell differentiation, but did result in the loss of the radial arrangement of RPCs and caused abnormal migration of differentiated neurons. As a result, the laminar structure was massively disrupted in beta-catenin-null retinas, although all retinal cell types still formed. In contrast to other neural tissues, eliminating beta-catenin did not significantly reduce the proliferation rate of RPCs; likewise, activating beta-catenin ectopically in RPCs did not result in overproliferation, but loss of neural retinal identity. These results indicate that beta-catenin is essential during retinal neurogenesis as a regulator of cell adhesion but not as a nuclear effector of the canonical Wnt signaling pathway. The results further imply that retinal lamination and retinal cell differentiation are genetically separable processes. |
