Special Focus Research Article
Shh signaling in limb bud ectoderm: Potential role in teratogen-induced postaxial ectrodactyly
Article first published online: 27 APR 2005
Copyright © 2005 Wiley-Liss, Inc.
Special Issue: Special Focus on Limb Development
Volume 233, Issue 2, pages 313–325, June 2005
How to Cite
Bell, S. M., Schreiner, C. M., Goetz, J. A., Robbins, D. J. and Scott, W. J. (2005), Shh signaling in limb bud ectoderm: Potential role in teratogen-induced postaxial ectrodactyly. Dev. Dyn., 233: 313–325. doi: 10.1002/dvdy.20409
- Issue published online: 12 MAY 2005
- Article first published online: 27 APR 2005
- Manuscript Revised: 25 FEB 2005
- Manuscript Accepted: 25 FEB 2005
- Manuscript Received: 9 NOV 2004
- NIH. Grant Number: ES11750
- polarizing activity;
A variety of teratogens induce the loss of postaxial forelimb structures when administered during mid-gestation to the mouse. Previous studies demonstrated that teratogen exposure is associated with a reduction in zone of polarizing activity (ZPA) -related polarizing activity without a noticeable loss of Shh expression. Herein, we quantitatively confirm that expression of Shh, Ptch1, and Gli3 are unaltered by teratogen exposure and demonstrate that sonic hedgehog (Shh) translation is unaffected. Examination of the polarizing response of host chick wings to teratogen-exposed ZPA tissue revealed an induced growth response and ectopic induction of Fgf4, Bmp2, Ptch1, and Gli1 expression similar to control ZPA tissue. Control ZPA tissue altered the fate of cells destined to die in the anterior necrotic zone, whereas cell death ensued in hosts receiving teratogen-exposed grafts. Immunohistochemical studies localized Shh protein in the mouse limb to the posterior mesoderm and overlying ectoderm. We postulate that teratogen exposure alters the ability of Shh to signal to the ectoderm and present microarray and reverse transcriptase-polymerase chain reaction data, indicating that Shh signaling could occur in the limb bud ectoderm. Developmental Dynamics 233:313–325, 2005. © 2005 Wiley-Liss, Inc.