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First published online 17 January 2007
doi: 10.1242/dev.02773
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1 Department of Molecular Biology and Pharmacology and Department of Medicine at
Washington University School of Medicine, 660 South Euclid Avenue, Campus Box
8103, St Louis, MO 63110, USA.
2 Department of Molecular and Cellular Biology, Harvard University, 16 Divinity
Avenue, Cambridge, MA 02138, USA.
3 Institute for Molecular Biology OE5250, Medizinische Hochschule Hannover,
Carl-Neuberg-Str. 1 D-30625 Hannover, Germany.
* Author for correspondence (e-mail: kopan{at}wustl.edu)
Accepted 5 December 2006
The Notch pathway regulates cell fate determination in numerous
developmental processes. Here we report that Notch2 acts non-redundantly to
control the processes of nephron segmentation through an Rbp-J-dependent
process. Notch1 and Notch2 are detected in the early renal vesicle. Genetic
analysis reveals that only Notch2 is required for the differentiation of
proximal nephron structures (podocytes and proximal convoluted tubules)
despite the presence of activated Notch1 in the nuclei of putative proximal
progenitors. The inability of endogenous Notch1 to compensate for Notch2
deficiency may reflect sub-threshold Notch1 levels in the nucleus. In line
with this view, forced expression of a 
-secretase-independent form of
Notch1 intracellular domain drives the specification of proximal fates where
all endogenous, ligand-dependent Notch signaling is blocked by a
-secretase inhibitor. These results establish distinct (non-redundant),
instructive roles for Notch receptors in nephron segmentation.
Key words: Notch, Rbp-J, Wnt4, Proximal tubule, Podocytes, Nephron segmentation, Mouse
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