Due to necessary maintenance, Xenbase will be unavailable December 24-30, 2014. We apologize for the inconvenience.

Click on this message to dismiss it.
Click here to close Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly. We suggest using a current version of Chrome, FireFox, or Safari.
XB-ART-36127
Dev Dyn. August 1, 2007; 236 (8): 2050-61.

Xenopus Lefty requires proprotein cleavage but not N-linked glycosylation to inhibit nodal signaling.

Westmoreland JJ , Takahashi S , Wright CV .


Abstract
The Nodal and Nodal-related morphogens are utilized for the specification of distinct cellular identity throughout development by activating discrete target genes in a concentration-dependant manner. Lefty is a principal extracellular antagonist involved in the spatiotemporal regulation of the Nodal morphogen gradient during mesendoderm induction. The Xenopus Lefty proprotein contains a single N-linked glycosylation motif in the mature domain and two potential cleavage sites that would be expected to produce long (Xlefty(L)) and short (Xlefty(S)) isoforms. Here we demonstrate that both isoforms were secreted from Xenopus oocytes, but that Xlefty(L) is the only isoform detected when embryonic tissue was analyzed. In mesoderm induction assays, Xlefty(L) is the functional blocker of Xnr signaling. When secreted from oocytes, vertebrate Lefty molecules were N-linked glycosylated. However, glycan addition was not required to inhibit Xnr signaling and did not influence its movement through the extracellular space. These findings demonstrate that Lefty molecules undergo post-translational modifications and that some of these modifications are required for the Nodal inhibitory function.

PubMed ID: 17584861
Article link: Dev Dyn.
Grant support: GM56238 NIGMS NIH HHS

Genes referenced: gal.2 gsc lefty myc nodal nodal2 odc1
Antibodies referenced:
Morpholinos referenced:
Article Images: [+] show captions

My Xenbase: [ Log-in / Register ]
version: [3.3.1]


Major funding for Xenbase is provided by the National Institute of Child Health and Human Development, grant P41 HD064556