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.

Developmental Dynamics : an Official Publication of the American Association of Anatomists
Rita De GasperiGregory A Elder

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.

References

Oct 14, 1994·Brain Research. Developmental Brain Research·D M WeisenhornM R Celio
Oct 9, 1995·The Journal of Comparative Neurology·M FonsecaE Soriano
Jun 10, 1998·The Journal of Comparative Neurology·Y T Kwon, L H Tsai
Feb 22, 2000·Biological Psychiatry·P H St George-Hyslop
Feb 13, 2001·The European Journal of Neuroscience·S KesavapanyC C Miller
Aug 25, 2001·Annual Review of Neuroscience·D S Rice, T Curran
May 4, 2002·Nature Reviews. Genetics·Amitabh GuptaAnthony Wynshaw-Boris
Jun 12, 2002·Molecular and Cellular Neurosciences·Kwok-Fai LauChristopher C J Miller
Oct 12, 2002·The Journal of Biological Chemistry·Uwe BeffertJoachim Herz
Jul 23, 2003·The Journal of Biological Chemistry·Petra MayJoachim Herz
May 28, 2004·Development·Angeliki LouviElizabeth A Grove
Jun 15, 2004·Current Opinion in Neurobiology·Takeshi Iwatsubo
Jul 16, 2004·Developmental Dynamics : an Official Publication of the American Association of Anatomists·Mitsunari NakajimaTakuji Shirasawa
Nov 3, 2004·Neuroscience Letters·Paul H WenGregory A Elder
Dec 25, 2004·Developmental Biology·Mary Wines-SamuelsonJie Shen
Jun 14, 2005·Brain Research. Molecular Brain Research·Hyang-Sook Hoe, G William Rebeck
Nov 4, 2005·Epilepsy & Behavior : E&B·Gabriella D'Arcangelo
Jan 18, 2006·Development·Michio YoshidaElizabeth A Grove
Aug 26, 2006·Molecular Neurodegeneration·Kulandaivelu S VetrivelGopal Thinakaran
Oct 21, 2006·Nature Reviews. Neuroscience·Joachim Herz, Ying Chen
Jan 16, 2007·Cell·Ramsés AyalaLi-Huei Tsai
Jan 16, 2007·Neurobiology of Aging·Han ZhangYun-wu Zhang
Aug 25, 2007·The Journal of Biological Chemistry·Emanuela RepettoDavid E Kang
Sep 14, 2007·Journal of Alzheimer's Disease : JAD·Mithu Raychaudhuri, Debashis Mukhopadhyay
Jan 10, 2008·Molecular Neurodegeneration·Woo-Young Kim, Jie Shen

❮ Previous
Next ❯

Citations

Dec 18, 2013·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Valeria BalmacedaJavier Sáez-Valero

❮ Previous
Next ❯

Related Concepts

Related Feeds

Cell Adhesion Molecules in the Brain

Cell adhesion molecules found on cell surface help cells bind with other cells or the extracellular matrix to maintain structure and function. Here is the latest research on their role in the brain.

AKT Pathway

This feed focuses on the AKT serine/threonine kinase, which is an important signaling pathway involved in processes such as glucose metabolism and cell survival.