期刊
SCIENCE
卷 307, 期 5707, 页码 265-268出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1105416
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资金
- NCI NIH HHS [CA23767-24] Funding Source: Medline
- NIMH NIH HHS [MH59199-06] Funding Source: Medline
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.
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