| First Author | Nelson BR | Year | 2009 |
| Journal | Dev Dyn | Volume | 238 |
| Issue | 9 | Pages | 2163-78 |
| PubMed ID | 19191219 | Mgi Jnum | J:151457 |
| Mgi Id | MGI:4353883 | Doi | 10.1002/dvdy.21848 |
| Citation | Nelson BR, et al. (2009) Acheate-scute like 1 (Ascl1) is required for normal delta-like (Dll) gene expression and notch signaling during retinal development. Dev Dyn 238(9):2163-2178 |
| abstractText | Delta gene expression in Drosophila is regulated by proneural basic helix-loop-helix (bHLH) transcription factors, such as acheate-scute. In vertebrates, multiple Delta-like and proneural bHLH genes are expressed during neurogenesis, especially in the retina. We recently uncovered a relationship between Acheate-scute like 1 (Ascl1), Delta-like genes, and Notch in chick retinal progenitors. Here, we report that mammalian retinal progenitors are also the primary source of Delta-like genes, likely signaling through Notch among themselves, while differentiating neurons expressed Jagged2. Ascl1 is coexpressed in Delta-like and Notch active progenitors, and required for normal Delta-like gene expression and Notch signaling. We also reveal a role for Ascl1 in the regulation of Hes6, a proneurogenic factor that inhibits Notch signaling to promote neural rather than glial differentiation. Thus, these results suggest a molecular mechanism whereby attenuated Notch levels coupled with reduced proneurogenic activity in progenitors leads to increased gliogenesis and decreased neurogenesis in the Ascl1-deficient retina. Developmental Dynamics 238:2163-2178, 2009. (c) 2009 Wiley-Liss, Inc. |
