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Published online before print May 2, 2003, 10.1101/gad.1084703
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Vol. 17, No. 10, pp. 1207-1212, May 15, 2003

RESEARCH COMMUNICATION
Notch signaling regulates left-right asymmetry determination by inducing Nodal expression

Luke T. Krebs,1,4 Naomi Iwai,2,3,4 Shigenori Nonaka,2,3 Ian C. Welsh,1 Yu Lan,1,5 Rulang Jiang,1,5 Yukio Saijoh,2 Timothy P. O'Brien,1 Hiroshi Hamada,2,3,6 and Thomas Gridley1,7

1 The Jackson Laboratory, Bar Harbor, Maine 04609, USA; 2 Developmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, Osaka 565-0871, Japan; 3 CREST (Core Research for Evolutional Science and Technology), Japan Science and Technology Corporation (JST), Osaka 565-0871, Japan

Generation of left-right asymmetry is an integral part of the establishment of the vertebrate body plan. Here we show that the Notch signaling pathway plays a primary role in the establishment of left-right asymmetry in mice by directly regulating expression of the Nodal gene. Embryos mutant for the Notch ligand Dll1 or doubly mutant for the Notch1 and Notch2 receptors exhibit multiple defects in left-right asymmetry. Analysis of the enhancer regulating node-specific Nodal expression revealed the presence of binding sites for the RBP-J protein, the primary transcriptional mediator of Notch signaling. Mutation of these sites destroyed the ability of this enhancer to direct node-specific gene expression in transgenic mice. Our results demonstrate that Dll1-mediated Notch signaling is essential for generation of left-right asymmetry, and that the Notch pathway acts upstream of Nodal expression during left-right asymmetry determination in mice.

[Keywords: Notch signaling; Dll1; left-right determination; Nodal]

4 These authors contributed equally to this work.

5 Present address: Center for Oral Biology, University of Rochester,

6 E-MAIL hamada{at}fbs.osaka-u.ac.jp; FAX 81-6-6878-9846.

7 E-MAIL gridley{at}jax.org; FAX (207) 288-6077.

© 2003 by Cold Spring Harbor Laboratory Press  ISSN 0890-9369/03 $5.00
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