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

Huang, C.C., Wang, T.C., Lin, B.H., Wang, Y.W., Johnson, S.L., and Yu, J.
Developmental Biology   332(2): 360-370 (Journal)
Registered Authors
Huang, Cheng-Chen, Johnson, Stephen L.
zebrafish, vascular plexus, collagen IX, actinotrichia, fin
MeSH Terms
  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Collagen Type II/chemistry
  • Collagen Type II/genetics
  • Collagen Type II/metabolism*
  • Collagen Type IX/chemistry
  • Collagen Type IX/genetics
  • Collagen Type IX/metabolism*
  • Extracellular Matrix/chemistry
  • Extracellular Matrix/metabolism
  • Extremities*/blood supply
  • Extremities*/embryology
  • Extremities*/growth & development
  • Female
  • In Situ Hybridization
  • Male
  • Models, Biological
  • Molecular Sequence Data
  • Morphogenesis/physiology
  • Neovascularization, Physiologic*
  • Point Mutation
  • Regeneration/physiology
  • Zebrafish*/anatomy & histology
  • Zebrafish*/embryology
  • Zebrafish*/growth & development
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
19501583 Full text @ Dev. Biol.
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
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Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes