Interaction of reelin signaling and Lis1 in brain development

2003 ◽  
Vol 35 (3) ◽  
pp. 270-276 ◽  
Author(s):  
Amir H Assadi ◽  
Guangcheng Zhang ◽  
Uwe Beffert ◽  
Robert S McNeil ◽  
Amy L Renfro ◽  
...  
Keyword(s):  
Brain Development ◽  
Reelin Signaling

A hypomorphic allele of dab1 reveals regional differences in reelin-Dab1 signaling during brain development

Development ◽  
2002 ◽  
Vol 129 (3) ◽  
pp. 787-796
Author(s):  
Tara M. Herrick ◽  
Jonathan A. Cooper
Keyword(s):  
Brain Development ◽  
Tyrosine Phosphorylation ◽  
Marginal Zone ◽  
Normal Development ◽  
Single Copy ◽  
Terminal Region ◽  
Cortical Plate ◽  
Phosphorylation Sites ◽  
Ca1 Region ◽  
Reelin Signaling

The disabled 1 (Dab1) p80 protein is essential for reelin signaling during brain development. p80 has an N-terminal domain for association with reelin receptors, followed by reelin-dependent tyrosine phosphorylation sites and about 310 C-terminal residues of unknown function. We have generated mutant mice that express only a natural splice form of Dab1, p45, that lacks the C-terminal region of p80. The normal development of these mice implies that the receptor-binding region and tyrosine phosphorylation sites of p80 are sufficient for reelin signaling. However, a single copy of the truncated gene does not support normal development of the neocortex and hippocampus. The CA1 region of the hippocampus is split into two well-organized layers, while the marginal zone of the neocortex is invaded by late-born cortical plate neurons. The haploinsufficiency of the p45 allele of Dab1 implies that the C terminus of p80 affects the strength of reelin-Dab1 signaling, yet there is no apparent change in reelin-dependent tyrosine phosphorylation of p45 relative to p80. Therefore, we suggest that the C-terminal region of Dab1 p80 is involved in signaling to downstream effector molecules. Furthermore, the presence of late-born cortical plate neurons in the marginal zone reveals a requirement for reelin-Dab1 signaling in late-born cortical plate neurons, and helps distinguish models for the cortical inversion in the reeler mutant mouse.

Reelin regulates differentiation of neural stem cells by activation of notch signaling through Disabled-1 tyrosine phosphorylation

2012 ◽  
Vol 90 (3) ◽  
pp. 361-369 ◽  
Author(s):  
Serene Keilani ◽  
DeLacy Healey ◽  
Kiminobu Sugaya
Keyword(s):  
Brain Development ◽  
Tyrosine Phosphorylation ◽  
Cell Fate ◽  
Molecular Mechanisms ◽  
Neural Progenitor Cells ◽  
Lipid Binding ◽  
Notch 1 ◽  
Radial Glial Cells ◽  
Human Neural Progenitor Cells ◽  
Reelin Signaling

We have previously reported the cross-talk between Reelin and Notch-1 signaling pathways, which are 2 major pathways that regulate brain development. We found that Reelin activated Notch-1 signaling, leading to the expression of brain lipid binding protein (BLBP) and the formation of radial glial cells in human neural progenitor cells (hNPCs). In the current study, we investigated the molecular mechanisms by which Reelin activates Notch-1. We show that Reelin-stimulated Notch-1 activation is dependent on Reelin signaling. The induction of Disabled-1 (Dab-1) tyrosine phosphorylation, and the subsequent activation of Src family kinases, were found to be essential steps for the activation of Notch-1 signaling by Reelin. Reelin treatment increased the interaction between Dab-1 and Notch-1 intracellular domain (NICD), and enhanced NICD translocation to the nucleus. This study advances our knowledge of the regulation of Notch-1 activation by Reelin signaling in hNPCs, as an approach to understanding cell fate determination, differentiation, and neurogenesis during brain development.

Chemical Contamination of Brain Development

1988 ◽  
Vol 33 (11) ◽  
pp. 992-993
Author(s):  
Bernard Weiss
Keyword(s):  
Brain Development ◽  
Chemical Contamination
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