期刊
NEURON
卷 110, 期 24, 页码 4074-+出版社
CELL PRESS
DOI: 10.1016/j.neuron.2022.12.005
关键词
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资金
- DFG [394046768-SFB 1366, SFB1366, SFB1158]
- state of Baden-Wurttemberg Foundation
- British Heart Foundation [FS/19/29/34367, FS/14/67/31294]
- European Research Council [864875, 335590]
- Giovanni Armenise-Harvard Foundation
- Wellcome [205099/Z/16/Z]
- University of Bonn
- Wellcome Trust [205099/Z/16/Z] Funding Source: Wellcome Trust
- European Research Council (ERC) [335590, 864875] Funding Source: European Research Council (ERC)
This study reveals the importance of communication between motor neurons and endothelial cells in spinal cord development, and the role of semaphorin 3C and PlexinD1 in regulating this process.
How the vascular and neural compartment cooperate to achieve such a complex and highly specialized structure as the central nervous system is still unclear. Here, we reveal a crosstalk between motor neurons (MNs) and endothelial cells (ECs), necessary for the coordinated development of MNs. By analyzing cell -to-cell interaction profiles of the mouse developing spinal cord, we uncovered semaphorin 3C (Sema3C) and PlexinD1 as a communication axis between MNs and ECs. Using cell-specific knockout mice and in vitro assays, we demonstrate that removal of Sema3C in MNs, or its receptor PlexinD1 in ECs, results in premature and aberrant vascularization of MN columns. Those vascular defects impair MN axon exit from the spinal cord. Impaired PlexinD1 signaling in ECs also causes MN maturation defects at later stages. This study highlights the importance of a timely and spatially controlled communication between MNs and ECs for proper spinal cord development.
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