PUBLICATION

The type I serine/threonine kinase receptor Alk8/Lost-a-fin is required for Bmp2b/7 signal transduction during dorsoventral patterning of the zebrafish embryo

Authors
Bauer, H., Lele, Z., Rauch, G.J., Geisler, R., and Hammerschmidt, M.
ID
ZDB-PUB-010306-5
Date
2001
Source
Development (Cambridge, England)   128(6): 849-858 (Journal)
Registered Authors
Bauer, Hermann, Geisler, Robert, Hammerschmidt, Matthias, Lele, Zsolt, Rauch, Gerd-Jörg
Keywords
Alk8; Bmp2b; Bmp7; Smad5; dorsoventral patterning; lost-a-fin; zebrafish; morpholino antisense oligonucleotides
MeSH Terms
  • Cloning, Molecular
  • Phenotype
  • Transforming Growth Factor beta*
  • Mutagenesis
  • Reverse Transcriptase Polymerase Chain Reaction
  • Genetic Linkage
  • Receptors, Transforming Growth Factor beta/genetics
  • Receptors, Transforming Growth Factor beta/physiology
  • Bone Morphogenetic Protein 7
  • Embryo, Nonmammalian/physiology*
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Signal Transduction/physiology*
  • Phylogeny
  • Activin Receptors
  • Zebrafish Proteins*
  • Animals
  • Crosses, Genetic
  • Protein Serine-Threonine Kinases/genetics
  • Protein Serine-Threonine Kinases/physiology*
  • Body Patterning/physiology*
  • Bone Morphogenetic Protein 2
  • Bone Morphogenetic Proteins/physiology*
  • Genotype
  • Transcription, Genetic
(all 25)
PubMed
11222140 Full text @ Development
Abstract
Ventral specification of mesoderm and ectoderm depends on signaling by members of the bone morphogenetic protein (Bmp) family. Bmp signals are transmitted by a complex of type I and type II serine/threonine kinase transmembrane receptors. Here, we show that Alk8, a novel member of the Alk1 subgroup of type I receptors, is disrupted in zebrafish lost-a-fin (laf) mutants. Two alk8/laf null alleles are described. In laf(tm110), a conserved extracellular cysteine residue is replaced by an arginine, while in laf(m100), Alk8 is prematurely terminated directly after the transmembrane domain. The zygotic effect of both mutations leads to dorsalization of intermediate strength. A much stronger dorsalization, simlar to that of bmp2b/swirl and bmp7/snailhouse mutants, however, is obtained by inhibiting both maternally and zygotically supplied alk8 gene products with morpholino antisense oligonucleotides. The phenotype of laf mutants and alk8 morphants can be rescued by injected mRNA encoding Alk8 or the Bmp-regulated transcription factor Smad5, but not by mRNA encoding Bmp2b or Bmp7. Conversely, injected mRNA encoding a constitutively active version of Alk8 can rescue the strong dorsalization of bmp2b/swirl and bmp7/snailhouse mutants, whereas smad5/somitabun mutant embryos do not respond. Altogether, the data suggest that Alk8 acts as a Bmp2b/7 receptor upstream of Smad5.
Genes / Markers
Figures
Figure Gallery (4 images)
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
dtc24
    Point Mutation
    m100
      Point Mutation
      ta72a
        Point Mutation
        tm110b
          Point Mutation
          ty68a
            Point Mutation
            1 - 5 of 5
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            Human Disease / Model
            No data available
            Sequence Targeting Reagents
            Target Reagent Reagent Type
            acvr1lMO1-acvr1lMRPHLNO
            acvr1lMO2-acvr1lMRPHLNO
            bmp2bMO1-bmp2bMRPHLNO
            1 - 3 of 3
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            Fish
            Antibodies
            No data available
            Orthology
            No data available
            Engineered Foreign Genes
            No data available
            Mapping
            Entity Type Entity Symbol Location
            Featurem100Chr: 2 Details
            Featuretm110bChr: 2 Details
            GENEacvr1lChr: 2 Details
            SSLPz9234Chr: 2 Details
            SSLPz17291Chr: 2 Details
            1 - 5 of 5
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