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

Science (New York, N.Y.) | Jan 14, 2005

http://www.ncbi.nlm.nih.gov/pubmed/15550623

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 RIS Download

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

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Associated grants

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

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