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.
Dev Dyn October 1, 2007; 236 (10): 2731-41.

The role of FoxC1 in early Xenopus development.

Cha JY , Birsoy B , Kofron M , Mahoney E , Lang S , Wylie C , Heasman J .

FoxC1 is an important transcription factor in vertebrate development since its mutation in humans results in Axenfeld-Rieger syndrome. In the mouse, disturbance of its function causes congenital hydrocephalus and abnormalities in the development of various mesodermal derivatives. In this report, we provide one mechanistic basis for the requirement for FoxC1 in vertebrate development. We find that, in Xenopus laevis embryos, FoxC1 expression is regulated by the maternal T-box transcription factor VegT, via the nodal sub-family of TGFbeta signaling transducers. We show that at the late neurula to early tailbud stage, FoxC1 depletion causes the down-regulation of adhesion molecules, EP and E cadherin, as well as members of the Ephrin/EphR signaling families in the mesoderm germ layer resulting in the loss of adhesion and apoptosis of mesodermal cells.

PubMed ID: 17705306
Article link: Dev Dyn
Grant support: R01 HD38272 NICHD NIH HHS

Genes referenced: ephb2 fgf8 foxc1 gata5 myod1 nodal nodal1 ocln odc1 rbfox1 sox17a tal1 tgfb1 vegt

Morpholinos referenced: foxc1 MO1

External Resources:
Article Images: [+] show captions

Xenbase: The Xenopus laevis and X. tropicalis resource.
Version: 4.9.2
Major funding for Xenbase is provided by the National Institute of Child Health and Human Development, grant P41 HD064556