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Semaphorin 3E and plexin-D1 control vascular pattern independently of neuropilins.

The development of a patterned vasculature is essential for normal organogenesis. We found that signaling by semaphorin 3E (Sema3E) and its receptor plexin-D1 controls endothelial cell positioning and the patterning of the developing vasculature in the mouse. Sema3E is highly expressed in developing somites, where it acts as a repulsive cue for plexin-D1-expressing endothelial cells of adjacent intersomitic vessels. Sema3E-plexin-D1 signaling did not require neuropilins, which were previously presumed to be obligate Sema3 coreceptors. Moreover, genetic ablation of Sema3E or plexin-D1 but not neuropilin-mediated Sema3 signaling disrupted vascular patterning. These findings reveal an unexpected semaphorin signaling pathway and define a mechanism for controlling vascular patterning.

Pubmed ID: 15550623


  • Gu C
  • Yoshida Y
  • Livet J
  • Reimert DV
  • Mann F
  • Merte J
  • Henderson CE
  • Jessell TM
  • Kolodkin AL
  • Ginty DD


Science (New York, N.Y.)

Publication Data

January 14, 2005

Associated Grants

  • Agency: NCI NIH HHS, Id: CA23767-24
  • Agency: NIMH NIH HHS, Id: MH59199-06

Mesh Terms

  • Animals
  • Binding Sites
  • Blood Vessels
  • Body Patterning
  • COS Cells
  • Cercopithecus aethiops
  • Chick Embryo
  • Endothelial Cells
  • Endothelium, Vascular
  • Glycoproteins
  • In Situ Hybridization
  • Ligands
  • Membrane Glycoproteins
  • Membrane Proteins
  • Mice
  • Morphogenesis
  • Mutation
  • Nerve Tissue Proteins
  • Neuropilin-1
  • Neuropilin-2
  • Phenotype
  • Protein Binding
  • Recombinant Fusion Proteins
  • Signal Transduction
  • Somites
  • Transfection