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

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Chenghua Gu; Yutaka Yoshida; Jean Livet; Dorothy V Reimert; Fanny Mann; Janna Merte; Christopher E Henderson; Thomas M Jessell; Alex L Kolodkin; David D Ginty (Profiled Authors: David Ginty; Alex Kolodkin)

Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2185, USA.
Science (New York, N.Y.) 2005;307(5707):265-8.

PubMed

Abstract

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.

Scientific Context

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