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

被引:400
作者
Gu, CH
Yoshida, Y
Livet, J
Reimert, DV
Mann, F
Merte, J
Henderson, CE
Jessell, TM
Kolodkin, AL [1 ]
Ginty, DD
机构
[1] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA
[2] Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Baltimore, MD 21205 USA
[3] Columbia Univ, Dept Biochem & Mol Biophys, Howard Hughes Med Inst, New York, NY 10032 USA
[4] Dev Biol Inst Marseille, INSERM, UMR623, F-13288 Marseille, France
关键词
D O I
10.1126/science.1105416
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 endotheiial 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.
引用
收藏
页码:265 / 268
页数:4
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