QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online 30 January 2008
doi: 10.1242/dev.010660

This Article Figures Only Full Text Full Text (PDF) Supplementary Material All Versions of this Article: dev.010660v1 135/5/919    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kinkel, M. D. Articles by Prince, V. E. Search for Related Content PubMed PubMed Citation Articles by Kinkel, M. D. Articles by Prince, V. E.

Cdx4 is required in the endoderm to localize the pancreas and limit β-cell number

Department of Organismal Biology and Anatomy, The University of Chicago, 1027 East 57th Street, Chicago, IL 60637, USA.

^* Author for correspondence (e-mail: mkinkel{at}uchicago.edu)

Accepted 15 December 2007

Cdx transcription factors have crucial roles in anteroposterior patterning of the nervous system and mesoderm. Here we focus on the role of cdx4 in patterning the endoderm in zebrafish. We show that cdx4 has roles in determining pancreatic β-cell number, directing midline convergence of β-cells during early pancreatic islet formation, and specifying the anteroposterior location of foregut organs. Embryos deficient in cdx4 have a posteriorly shifted pancreas, liver and small intestine. The phenotype is more severe with knockdown of an additional Cdx factor, cdx1a. We show that cdx4 functions within the endoderm to localize the pancreas. Morpholino knockdown of cdx4 specifically in the endoderm recapitulates the posteriorly shifted pancreas observed in cdx4 mutants. Conversely, overexpression of cdx4 specifically in the endoderm is sufficient to shift the pancreas anteriorly. Together, these results suggest a model in which cdx4 confers posterior identity to the endoderm. Cdx4 might function to block pancreatic identity by preventing retinoic acid (RA) signal transduction in posterior endoderm. In support of this, we demonstrate that in cdx4-deficient embryos treated with RA, ectopic β-cells are located well posterior to the normal pancreatic domain.

Key words: Cdx4, Cdx1a, Retinoic acid, Pancreas, β-cell, AP patterning

This article has been cited by other articles:

				T. F. Schilling Anterior-posterior patterning and segmentation of the vertebrate head Integr. Comp. Biol., August 5, 2008; (2008) icn081v1. [Abstract] [Full Text] [PDF]