PUBLICATION

Collagen IX is Required for the Integrity of Collagen II Fibrils and the Regulation of Vascular Plexus Formation in Zebrafish Caudal Fins

Authors
Huang, C.C., Wang, T.C., Lin, B.H., Wang, Y.W., Johnson, S.L., and Yu, J.
ID
ZDB-PUB-090616-31
Date
2009
Source
Developmental Biology   332(2): 360-370 (Journal)
Registered Authors
Huang, Cheng-Chen, Johnson, Stephen L.
Keywords
zebrafish, vascular plexus, collagen IX, actinotrichia, fin
MeSH Terms
  • Collagen Type IX/chemistry
  • Collagen Type IX/genetics
  • Collagen Type IX/metabolism*
  • Models, Biological
  • Extremities*/blood supply
  • Extremities*/embryology
  • Extremities*/growth & development
  • Male
  • Amino Acid Sequence
  • Base Sequence
  • Zebrafish*/anatomy & histology
  • Zebrafish*/embryology
  • Zebrafish*/growth & development
  • Morphogenesis/physiology
  • Neovascularization, Physiologic*
  • Animals
  • Regeneration/physiology
  • Extracellular Matrix/chemistry
  • Extracellular Matrix/metabolism
  • Point Mutation
  • In Situ Hybridization
  • Molecular Sequence Data
  • Female
  • Collagen Type II/chemistry
  • Collagen Type II/genetics
  • Collagen Type II/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
(all 28)
PubMed
19501583 Full text @ Dev. Biol.
Abstract
Capillary plexuses form during both vasculogenesis and angiogenesis and are remodeled into mature vessel types and patterns which are delicately orchestrated with the sizes and shapes of other tissues and organs. We isolated a zebrafish mutation named prp (for persistent plexus) that causes persistent formation of vascular plexuses in the caudal fins and consequent mispatterning of bony fin rays and the fin shape. Detailed analyses revealed that the prp mutation causes a significant reduction in the size and dramatic structural defects in collagen II-rich extracellular matrices called actinotrichia of both embryonic finfolds and adult fins. prp was mapped to chromosome 19 and found to encode the zebrafish collagen9alpha1 (col9alpha1) gene which is abundantly expressed in developing finfolds. A point mutation resulting in a leucine-to-histidine change was detected in the thrombospondin domain of the col9alpha1 gene in prp. Morpholino-mediated knockdown of col9alpha1 phenocopied the prp small finfold phenotype in wild-type embryos, and an injection of plasmids containing the col9alpha1 cDNA into prp embryos locally restored the finfold size. Furthermore, we found that osteoblasts in prp mutants were mispatterned apparently following the abnormal vascular plexus pattern, demonstrating that blood vessels play an important role in the patterning of bony rays in zebrafish caudal fins.
Genes / Markers
Marker Marker Type Name
col22a1GENEcollagen, type XXII, alpha 1
z3782SSLPZ3782
z40343SSLPz40343
z4825SSLPZ4825
z7450SSLPZ7450
1 - 5 of 5
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Figures
Figure Gallery (11 images) / 2
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
j131
    Point Mutation
    y1TgTransgenic Insertion
      1 - 2 of 2
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      Human Disease / Model
      No data available
      Sequence Targeting Reagents
      Target Reagent Reagent Type
      col22a1MO3-col22a1MRPHLNO
      1 - 1 of 1
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      Fish
      Antibodies
      Name Type Antigen Genes Isotypes Host Organism
      zn-8monoclonalIgG1Mouse
      zns-5monoclonal
        IgG1Mouse
        1 - 2 of 2
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        Orthology
        No data available
        Engineered Foreign Genes
        Marker Marker Type Name
        EGFPEFGEGFP
        1 - 1 of 1
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        Mapping
        Entity Type Entity Symbol Location
        SSLPz3782Chr: 19 Details
        SSLPz4825Chr: 19 Details
        SSLPz7450Chr: 19 Details
        SSLPz40343Chr: 19 Details
        1 - 4 of 4
        Show