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Dev Biol. 2006 Oct 15;298(2):514-26. Epub 2006 Jul 12.

Noggin1 and Follistatin-like2 function redundantly to Chordin to antagonize BMP activity.

Author information

1
Institut de Génétique et de Biologie Moléculaire et Cellulaire, UMR 7104, CNRS/INSERM/ULP, 1 rue Laurent Fries, BP 10142, CU de Strasbourg, 67404 ILLKIRCH Cedex, France.

Abstract

In Xenopus, the dorso-ventral (D/V) axis is thought to be specified by the bone morphogenetic proteins (Bmp) activity arising through interaction with antagonists such as Noggin, Chordin and Follistatin. We report here, through inactivation of noggin1 (nog1) that this gene is not essential by itself to establish the D/V patterning. However, at blastula stage, inactivation of nog1 strongly amplifies chordin (chd) phenotype, revealing redundant functions of these two genes on D/V axis formation. Substantial dorsal tissues remaining in the double nog1-chd morphant suggested that other anti-Bmp factors may pattern the D/V axis. We isolated two potential candidates, the follistatin-like (fstl) genes. We found that fstl2 is an early gastrula expressed gene. Its inactivation, similar to nog1, strongly enhances the chd phenotype. Moreover, the penetrance of the ventralization phenotype is much higher when we inactivated simultaneously chd, nog1 and fstl2. Altogether, our data reveal that, while Chordin is the main player of the D/V axis, sufficient to maintain proper activity of Bmp gradient, the structures remaining in the chd mutant (namely dorsal and dorso-lateral territories, in both mesodermal and ectodermal layers) result from the anti-Bmp activity carried by Nog1 and Fstl2 at blastula and gastrula stages.

PMID:
16890217
DOI:
10.1016/j.ydbio.2006.07.002
[Indexed for MEDLINE]
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