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First published online August 14, 2006
doi: 10.1242/10.1242/dev.02515

Development 133, 3277-3282 (2006)
Published by The Company of Biologists 2006
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A garden of Notch-ly delights

Gerry Weinmaster1,* and Raphael Kopan2

1 Department of Biological Chemistry, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1737, USA.
2 Department of Molecular Biology and Pharmacology, Washington University, St Louis, MO 63301, USA.


Figure 1
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  		Fig. 1. The Notch signaling pathway. The key players in this pathway are shown and consist of a Delta-type ligand, the receptor Notch and the CSL transcription factor. Delta and Notch are transmembrane proteins that contain extracellular arrays of EGF repeats (rectangles). The activation of Notch by its ligand triggers two proteolytic cleavages of Notch (S2 and S3). S3 cleavage releases the Notch intracellular domain (NICD, Notchintra), which translocates to the nucleus and then activates CSL. The CSL co-repressor complex is displaced by a coactivator complex, containing NICD (Co-A, green), which mediates Notch target gene activation. In the absence of nuclear NICD, CSL associates with a co-repressor complex (Co-R, red), which actively represses the transcription of Notch target genes. Reproduced, with permission, from Lai (Lai, 2004Go).

 

Figure 2
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  		Fig. 2. Notch pathway mutations and arteriovenous malformations. (A) In a wild-type mouse embryo, India ink injected into the heart in order to visualize blood flow exits through the aortic arch arteries and enters the descending dorsal aorta. (B) In an embryo with an endothelial cell-specific deletion of the Notch1 gene, the injected ink leaks directly into the venous system via arteriovenous malformations. Images courtesy of Luke Krebs and Tom Gridley.

 




© The Company of Biologists Ltd 2006