References
Query Results -- Details
MGI Accession ID: MGI:3806409
J Number: J:138800
Other Accession IDs:
Title: 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.
Authors: De Gasperi R; Gama Sosa MA; Wen PH; Li J; Perez GM; Curran T; Elder GA
Journal: Dev Dyn
Volume: 237
Issue: 9
Date: 2008 Sep
Year: 2008
Pages: 2405-14
Review Status: Peer Reviewed
Abstract:
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.
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