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Gewählte Publikation:

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Publikationstyp: Zeitschriftenaufsatz
Dokumenttyp: Originalarbeit

Jahr: 2007

AutorInnen: Brandt, N; Franke, K; Rasin, MR; Baumgart, J; Vogt, J; Khrulev, S; Hassel, B; Pohl, EE; Sestan, N; Nitsch, R; Schumacher, S

Titel: The neural EGF family member CALEB/NGC mediates dendritic tree and spine complexity.

Quelle: EMBO J. 2007; 26(9):2371-2386

Autor/innen der Vetmeduni Vienna:

Pohl Elena

Diese Publikation wurde nicht im Namen der Vetmeduni Vienna erstellt und ist deshalb ausschließlich der persönlichen Publikationsliste des/der Autors/Autorin zugeordnet!

The development of dendritic arborizations and spines is essential for neuronal information processing, and abnormal dendritic structures and/or alterations in spine morphology are consistent features of neurons in patients with mental retardation. We identify the neural EGF family member CALEB/NGC as a critical mediator of dendritic tree complexity and spine formation. Overexpression of CALEB/NGC enhances dendritic branching and increases the complexity of dendritic spines and filopodia. Genetic and functional inactivation of CALEB/NGC impairs dendritic arborization and spine formation. Genetic manipulations of individual neurons in an otherwise unaffected microenvironment in the intact mouse cortex by in utero electroporation confirm these results. The EGF-like domain of CALEB/NGC drives both dendritic branching and spine morphogenesis. The phosphatidylinositide 3-kinase (PI3K)-Akt-mammalian target of rapamycin (mTOR) signaling pathway and protein kinase C (PKC) are important for CALEB/NGC-induced stimulation of dendritic branching. In contrast, CALEB/NGC-induced spine morphogenesis is independent of PI3K but depends on PKC. Thus, our findings reveal a novel switch of specificity in signaling leading to neuronal process differentiation in consecutive developmental events.

Keywords Pubmed: Animals
Cells, Cultured
Dendritic Spines/physiology*
Embryo, Mammalian/cytology
Epidermal Growth Factor/genetics
Epidermal Growth Factor/physiology*
Membrane Proteins/genetics
Membrane Proteins/physiology*
Oncogene Protein v-akt/metabolism
Phosphatidylinositol 3-Kinases/metabolism
Protein Kinase C/metabolism
Protein Kinases/metabolism
Rats, Wistar
Signal Transduction
TOR Serine-Threonine Kinases

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