| First Author | De Gasperi R | Year | 2008 |
| Journal | Dev Dyn | Volume | 237 |
| Issue | 9 | Pages | 2405-14 |
| PubMed ID | 18729224 | Mgi Jnum | J:138800 |
| Mgi Id | MGI:3806409 | Doi | 10.1002/dvdy.21661 |
| Citation | De Gasperi R, et al. (2008) Cortical development in the presenilin-1 null mutant mouse fails after splitting of the preplate and is not due to a failure of reelin-dependent signaling. Dev Dyn 237(9):2405-14 |
| abstractText | Cortical development is disrupted in presenilin-1 null mutant (Psen1-/-) mice. Prior studies have commented on similarities between Psen1-/- and reeler mice. Reelin induces phosphorylation of Dab1 and activates the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Psen1 is known to modulate PI3K/Akt signaling and both known reelin receptors (apoER2 and VLDLR) are substrates for Psen1 associated gamma-secretase activity. The purpose of this study was to determine whether reelin signaling is disrupted in Psen1-/- mice. We show that, while Dab1 is hypophosphorylated late in cortical development in Psen1-/- mice, it is normally phosphorylated at earlier ages and reelin signaling is intact in Psen1-/- primary neuronal cultures. gamma-secretase activity was also not required for reelin-induced phosphorylation of Dab1. Unlike reeler mice the preplate splits in Psen1-/- brain. Thus cortical development in Psen1-/- mice fails only after splitting of the preplate and is not due to an intrinsic failure of reelin signaling. Developmental Dynamics 237:2405-2414, 2008. (c) 2008 Wiley-Liss, Inc. |
