|ZFIN ID: ZDB-PUB-050318-10|
Regulation of the early expression patterns of the zebrafish Dishevelled-interacting proteins Dapper1 and Dapper2
|Source:||Developmental dynamics : an official publication of the American Association of Anatomists 233(1): 194-200 (Journal)|
|Registered Authors:||Waxman, Joshua|
|Keywords:||Dapper1, Dapper2, beta-catenin, Nodal, Boz, BMP, zebrafish|
|PubMed:||15765513 Full text @ Dev. Dyn.|
Waxman, J.S. (2005) Regulation of the early expression patterns of the zebrafish Dishevelled-interacting proteins Dapper1 and Dapper2. Developmental dynamics : an official publication of the American Association of Anatomists. 233(1):194-200.
ABSTRACTThe Dapper/Frodo family of proteins are Dishevelled-interacting regulators of Wnt signaling. In this study, I characterize the regulation of the early expression patterns of dpr1 and dpr2. Although both dpr1 and dpr2 are expressed on the prospective dorsal side, I find that their pregastrula expression patterns have differences that have not been reported previously. Early dpr1 expression is much more dynamic than dpr2 expression. I use gain and loss of function experiments to identify dorsal organizer genes that regulate dpr1 and dpr2 expression. The dorsalizing factors beta-catenin, Bozozok (Boz), Noggin (Nog), and the mesendoderm-inducing factor Squint (Sqt) are all able to induce ectopic expression of dpr1 and dpr2. In reciprocal loss of function experiments, loss of maternal beta-catenin signaling leads to loss of early dorsal dpr1 and dpr2 expression, whereas loss of Boz and/or Nodal signaling does not. Ectopic expression of the ventralizing molecule Bmp2b leads to reduction of dpr1 and dpr2 expression. These results suggest that, in early zebrafish development, dpr1 and dpr2 are targets of beta-catenin and/or an unknown downstream effector. Their expression from 30% epiboly through shield is maintained by Nodal signaling and likely refined by the mutually antagonistic effects of Boz and bone morphogenetic protein signaling. Developmental Dynamics, 2005. (c) 2005 Wiley-Liss, Inc.