% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Vieira:186452,
      author       = {J. R. Vieira and B. Shah and S. Dupraz and I. Paredes and
                      P. Himmels and G. Schermann and H. Adler and A. Motta and L.
                      Gärtner and A. Navarro-Aragall and E. Ioannou and E.
                      Dyukova and R. Bonnavion and A. Fischer$^*$ and D. Bonanomi
                      and F. Bradke and C. Ruhrberg and C. Ruiz de Almodóvar},
      title        = {{E}ndothelial {P}lexin{D}1 signaling instructs spinal cord
                      vascularization and motor neuron development.},
      journal      = {Neuron},
      volume       = {110},
      number       = {24},
      issn         = {0896-6273},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2022-03173},
      pages        = {4074 - 4089.e6},
      year         = {2022},
      abstract     = {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.},
      keywords     = {Animals / Mice / Endothelial Cells / Motor Neurons:
                      physiology / Spinal Cord / Signal Transduction / Axons /
                      Mice, Knockout / CNS vascularization (Other) / PlexinD1
                      (Other) / Sema3C (Other) / blood vessel (Other) /
                      endothelial cell (Other) / motor neuron (Other) /
                      neuro-vascular communication (Other) / neurodevelopment
                      (Other) / spinal cord (Other)},
      cin          = {A270},
      ddc          = {610},
      cid          = {I:(DE-He78)A270-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36549270},
      doi          = {10.1016/j.neuron.2022.12.005},
      url          = {https://inrepo02.dkfz.de/record/186452},
}