Nodal activity in the node governs left-right asymmetry.
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.
Brennan
Jane
J
Department of Molecular and Cellular Biology, Harvard University, The Biological Laboratories, Cambridge, Massachusetts 02138, USA.
Norris
Dominic P
DP
Robertson
Elizabeth J
EJ
D000818:Animals; D001483:Base Sequence; D019521:Body Patterning / Q000235:genetics* / Q000502:physiology*; D004247:DNA / Q000235:genetics; D018507:Gene Expression Regulation, Developmental; D018390:Gene Targeting; D006801:Humans; D017403:In Situ Hybridization; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D055457:Nodal Protein; D020897:Organizers, Embryonic / Q000196:embryology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012689:Sequence Homology, Nucleic Acid; D015398:Signal Transduction; D016212:Transforming Growth Factor beta / Q000235:genetics* / Q000502:physiology*
C526007:NODAL protein, human; D055457:Nodal Protein; C526008:Nodal protein, mouse; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D004247:DNA