PUBLICATION

The zebrafish dyrk1b gene is important for endoderm formation

Authors
Mazmanian, G., Kovshilovsky, M., Yen, D., Mohanty, A., Mohanty, S., Nee, A., and Nissen, R.M.
ID
ZDB-PUB-091221-23
Date
2010
Source
Genesis (New York, N.Y. : 2000)   48(1): 20-30 (Journal)
Registered Authors
Nissen, Robert M.
Keywords
Mirk, dyrk1b, wdr68, craniofacial, edn1
MeSH Terms
  • Animals
  • DNA, Antisense/genetics
  • Embryo, Nonmammalian/embryology
  • Embryo, Nonmammalian/metabolism*
  • Endoderm/embryology
  • Endoderm/metabolism*
  • Gene Expression Regulation, Developmental
  • Gene Knockdown Techniques
  • In Situ Hybridization
  • Intracellular Signaling Peptides and Proteins/genetics
  • Intracellular Signaling Peptides and Proteins/metabolism
  • Left-Right Determination Factors/genetics
  • Nuclear Proteins/genetics
  • Protein-Tyrosine Kinases/genetics
  • Protein-Tyrosine Kinases/metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Zebrafish/embryology
  • Zebrafish/genetics*
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism
PubMed
20014342 Full text @ Genesis
Abstract
Nodal-signaling is required for specification of mesoderm, endoderm, establishing left-right asymmetry, and craniofacial development. Wdr68 is a WD40-repeat domain-containing protein recently shown to be required for endothelin-1 (edn1) expression and subsequent lower jaw development. Previous reports detected the Wdr68 protein in multiprotein complexes containing mammalian members of the dual-specificity tyrosine-regulated kinase (dyrk) family. Here we describe the characterization of the zebrafish dyrk1b homolog. We report the detection of a physical interaction between Dyrk1b and Wdr68. We also found perturbations of nodal signaling in dyrk1b antisense morpholino knockdown (dyrk1b-MO) animals. Specifically, we found reduced expression of lft1 and lft2 (lft1/2) during gastrulation and a near complete loss of the later asymmetric lft1/2 expression domains. Although wdr68-MO animals did not display lft1/2 expression defects during gastrulation, they displayed a near complete loss of the later asymmetric lft1/2 expression domains. While expression of ndr1 was not substantially effected during gastrulation, ndr2 expression was moderately reduced in dyrk1b-MO animals. Analysis of additional downstream components of the nodal signaling pathway in dyrk1b-MO animals revealed modestly expanded expression of the dorsal axial mesoderm marker gsc while the pan-mesodermal marker bik was largely unaffected. The endodermal markers cas and sox17 were also moderately reduced in dyrk1b-MO animals. Notably, and similar to defects previously reported for wdr68 mutant animals, we also found reduced expression of the pharyngeal pouch marker edn1 in dyrk1b-MO animals. Taken together, these data reveal a role for dyrk1b in endoderm formation and craniofacial patterning in the zebrafish.
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