PUBLICATION

No tail co-operates with non-canonical Wnt signaling to regulate posterior body morphogenesis in zebrafish

Authors
Marlow, F., Gonzalez, E.M., Yin, C., Rojo, C., and Solnica-Krezel, L.
ID
ZDB-PUB-080309-1
Date
2004
Source
Development (Cambridge, England)   131(1): 203-216 (Journal)
Registered Authors
Gonzalez, Encina, Marlow, Florence, Solnica-Krezel, Lilianna, Yin, Chunyue
Keywords
Convergence, Extension, Gastrulation, knypek, silberblick (wnt11), pipetail (wnt5), subduction
MeSH Terms
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Proto-Oncogene Proteins/physiology*
  • Embryo, Nonmammalian/physiology*
  • Phenotype
  • Gastrula/physiology*
  • Genotype
  • Zebrafish Proteins*
  • Mutation
  • Signal Transduction
  • Animals
  • Tail/abnormalities
  • Tail/embryology*
  • Movement/physiology
  • Gene Expression Regulation, Developmental/genetics*
  • Body Patterning/physiology
  • Morphogenesis/physiology*
  • Wnt Proteins
(all 18)
PubMed
14660439 Full text @ Development
Abstract
The vertebrate posterior body is formed by a combination of the gastrulation movements that shape the head and anterior trunk and posterior specific cell behaviors. Here, we investigated whether genes that regulate cell movements during gastrulation [no tail (ntl)/brachyury, knypek (kny) and pipetail (ppt)/wnt5] interact to regulate posterior body morphogenesis. Both kny;ntl and ppt;ntl double mutant embryos exhibit synergistic trunk and tail shortening by early segmentation. Gene expression analysis in the compound mutants indicates that anteroposterior germ-layer patterning is largely normal and that the tail elongation defects are not due to failure to specify or maintain posterior tissues. Moreover, ntl interacts with ppt and kny to synergistically regulate the posterior expression of the gene encoding bone morphogenetic protein 4 (bmp4) but not of other known T-box genes, fibroblast growth factor genes or caudal genes. Examination of mitotic and apoptotic cells indicates that impaired tail elongation is not simply due to decreased cell proliferation or increased cell death. Cell tracing in ppt;ntl and kny;ntl mutants demonstrates that the ventral derived posterior tailbud progenitors move into the tailbud. However, gastrulation-like convergence and extension movements and cell movements within the posterior tailbud are impaired. Furthermore, subduction movements of cells into the mesendoderm are reduced in kny;ntl and ppt;ntl mutants. We propose that Ntl and the non-canonical Wnt pathway components Ppt and Kny function in parallel, partially redundant pathways to regulate posterior body development. Our work initiates the genetic dissection of posterior body morphogenesis and links genes to specific tail-forming movements. Moreover, we provide genetic evidence for the notion that tail development entails a continuation of mechanisms regulating gastrulation together with mechanisms unique to the posterior body.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
b195
    Insertion
    m119
      Point Mutation
      ta98
        Point Mutation
        tz216
          Point Mutation
          1 - 4 of 4
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          Human Disease / Model
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          Sequence Targeting Reagents
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          Fish
          Antibodies
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          Orthology
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          Engineered Foreign Genes
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          Mapping
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