|
|
|
|
|
|
|
||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||
1 Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
2 Department of Biochemistry, University of Washington, Seattle, WA 98195, USA
3 Developmental Genetics Program, Skirball Institute of Biomolecular Medicine, Department of Cell Biology, New York University School of Medicine, New York, NY 10016, USA
* Present address: Molecular and Cellular Biology Program, University of Washington, Seattle, WA 98195, USA
Author for correspondence (e-mail: talbot{at}cmgm.stanford.edu)
Accepted March 26, 2001
Ventralizing transcriptional repressors in the Vox/Vent family have been proposed to be important regulators of dorsoventral patterning in the early embryo. While the zebrafish genes vox (vega1) and vent (vega2) both have ventralizing activity in overexpression assays, loss-of-function studies are needed to determine whether these genes have distinct or redundant functions in dorsoventral patterning and to provide critical tests of the proposed regulatory interactions among vox, vent and other genes that act to establish the dorsoventral axis. We show that vox and vent are redundant repressors of dorsal fates in zebrafish. Mutants that lack vox function have little or no dorsoventral patterning defect, and inactivation of either vox or vent by injection of antisense morpholino oligonucleotides has little or no effect on the embryo. In contrast, embryos that lack both vox and vent function have a dorsalized phenotype. Expression of dorsal mesodermal genes, including chordin, goosecoid and bozozok, is strongly expanded in embryos that lack vox and vent function, indicating that the redundant action of vox and vent is required to restrict dorsal genes to their appropriate territories. Our genetic analysis indicates that the dorsalizing transcription factor Bozozok promotes dorsal fates indirectly, by antagonizing the expression of vox and vent. In turn, vox and vent repress chordin expression, restricting its function as an antagonist of ventral fates to the dorsal side of the embryo. Our results support a model in which BMP signaling induces the expression of ventral genes, while vox and vent act redundantly to prevent the expression of chordin, goosecoid and other dorsal genes in the lateral and ventral mesendoderm.
Key words: vox, vent, bozozok, chordin, goosecoid, bmp, Gastrulation, Morpholino, Zebrafish
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati 
Twitter What's this?
This article has been cited by other articles:
|
|
 |
|
  R. Esterberg, J.-M. Delalande, and A. Fritz Tailbud-derived Bmp4 drives proliferation and inhibits maturation of zebrafish chordamesoderm Development, December 1, 2008; 135(23): 3891 - 3901. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S.-H. Shiu and A. B. Bleecker Plant Receptor-Like Kinase Gene Family: Diversity, Function, and Signaling Sci. Signal., December 18, 2001; 2001(113): re22 - re22. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. A. Henningfeld, H. Friedle, S. Rastegar, and W. Knochel Autoregulation of Xvent-2B; Direct Interaction and Functional Cooperation of Xvent-2 and Smad1 J. Biol. Chem., January 11, 2002; 277(3): 2097 - 2103. [Abstract] [Full Text] [PDF]
|
|
