| First Author | Ouchi Y | Year | 2011 |
| Journal | Mol Cell Neurosci | Volume | 46 |
| Issue | 4 | Pages | 770-80 |
| PubMed ID | 21354309 | Mgi Jnum | J:171283 |
| Mgi Id | MGI:4949560 | Doi | 10.1016/j.mcn.2011.02.010 |
| Citation | Ouchi Y, et al. (2011) beta-Catenin signaling regulates the timing of cell differentiation in mouse retinal progenitor cells. Mol Cell Neurosci 46(4):770-80 |
| abstractText | Wnt signaling is important in development and carcinogenesis. We previously showed that active beta-catenin or Lef-1 in the mammalian retinal culture prevents differentiation of retinal cells without modifying cellular proliferation. In this study, we investigated the in vivo role of beta-catenin in mouse retinal differentiation in transgenic mice, in which retinal-specific activation or inactivation of beta-catenin was achieved with Cre recombinase. The gain-of-function mice exhibited small eyes and large cell aggregates consisting of early progenitor cells labeled with SSEA-1 in the peripheral retina. In the loss-of-function mice, we observed a reduced number of SSEA-1-positive progenitor cells and the presence of differentiated cells in the beta-catenin ablated retinal region. Interestingly, the number of proliferating cells in the beta-catenin gain-of-function mice was highly downregulated, and the proliferation index detected by Ki67 expression was slightly lower than that of control mice in the beta-catenin loss-of-function mice. The Gsk-3beta inhibitor BIO induced expression of Id3, which was highly expressed in SSEA-1-positive cells, and transiently maintained SSEA-1-positive retinal progenitor cells (RPCs). Forced expression of Id3 in RPCs mimicked the effects of BIO. Taken together, beta-catenin signaling regulates the timing of differentiation in RPCs by inhibiting premature differentiation of them partly through the regulation of Id3 expression. |
