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

Authors:
Gu C, Yoshida Y, Livet J, Reimert DV, Mann F, Merte J, Henderson CE, Jessell TM, Kolodkin AL, Ginty DD
Associated Labs:
Ginty Lab (Johns Hopkins University and School of Medicine)
Science. 2005 Jan 14. 307(5707):265-8.
PMID: 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.

Want to be recognized as an author of this publication?

Create your LabLife profile and tag yourself! You will also be able to tag other authors after you log into your account.

Create New Account

Login

What is LabLife?

LabLife is a collection of tools to help scientists organize, share and discover.

Learn more