Nodal activity in the node governs left-right asymmetry
Abstract
Nodal is expressed at the lateral edges of the mouse node, but its function in this “organizer” tissue remains unknown due to the early lethality of Nodal mutant embryos. Here we used a genetic strategy to selectively remove Nodal activity from the node. Embryos lacking Nodal in the node fail to initiate molecular asymmetry in the left lateral plate mesoderm and exhibit multiple left-right patterning defects. Nodal may also act as a short-range signal to establish a functional midline barrier. Our findings confirm that the mouse node is instrumental in initiating left-right axis specification and identify Nodal as the key morphogen regulating this process.
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Footnotes
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Present addresses: 1Centre for Genome Research, University of Edinburgh, Edinburgh, EH9 3JQ, UK.; 2Medical Research Council Mammalian Genetics Unit, Harwell, Oxfordshire, OX11 0RD, UK.
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↵3 Corresponding author.
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E-MAIL ejrobert{at}fas.harvard.edu; FAX (617) 496-6770.
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Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.1016202.
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- Received June 18, 2002.
- Accepted August 1, 2002.
- Cold Spring Harbor Laboratory Press
