eprintid: 1558498
rev_number: 33
eprint_status: archive
userid: 608
dir: disk0/01/55/84/98
datestamp: 2017-06-03 21:34:42
lastmod: 2022-01-10 00:31:55
status_changed: 2017-07-21 11:22:40
type: article
metadata_visibility: show
creators_name: Bahm, I
creators_name: Barriga, EH
creators_name: Frolov, A
creators_name: Theveneau, E
creators_name: Frankel, P
creators_name: Mayor, R
title: PDGF controls contact inhibition of locomotion by regulating N-cadherin during neural crest migration
ispublished: pub
divisions: UCL
divisions: B02
divisions: C08
divisions: D09
divisions: F96
divisions: D14
divisions: GA2
keywords: Developmental Biology, PDGF, PDGFR, Neural Crest, EMT, Contact inhibition of locomotion, N-cadherin, Migration, Xenopus, COLLECTIVE CELL-MIGRATION, EPITHELIAL-MESENCHYMAL TRANSITIONS, ZEBRAFISH EMBRYONIC-DEVELOPMENT, GROWTH-FACTOR, CRANIOFACIAL DEVELOPMENT, SIGNALING PATHWAYS, IN-VIVO, XENOPUS-LAEVIS, ALPHA-RECEPTOR, MESSENGER-RNA
note: © 2017. Published by The Company of Biologists Ltd http://creativecommons.org/licenses/by/3.0
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
abstract: A fundamental property of neural crest (NC) migration is contact
inhibition of locomotion (CIL), a process by which cells change their
direction of migration upon cell contact. CIL has been proven to
be essential for NC migration in amphibians and zebrafish by
controlling cell polarity in a cell contact-dependent manner. Cell
contact during CIL requires the participation of the cell adhesion
molecule N-cadherin, which starts to be expressed by NC cells as a
consequence of the switch between E- and N-cadherins during
epithelial-to-mesenchymal transition (EMT). However, the mechanism
that controls the upregulation of N-cadherin remains unknown. Here,
we show that platelet-derived growth factor receptor alpha (PDGFRα)
and its ligand platelet-derived growth factor A (PDGF-A) are
co-expressed in migrating cranial NC. Inhibition of PDGF-A/PDGFRα
blocks NC migration by inhibiting N-cadherin and, consequently,
impairing CIL. Moreover, we identify phosphatidylinositol-3-kinase
(PI3K)/AKT as a downstream effector of the PDGFRα cellular
response during CIL. Our results lead us to propose PDGF-A/
PDGFRα signalling as a tissue-autonomous regulator of CIL by
controlling N-cadherin upregulation during EMT. Finally, we show that
once NC cells have undergone EMT, the same PDGF-A/PDGFRα
works as an NC chemoattractant, guiding their directional migration.
date: 2017-07-01
date_type: published
publisher: COMPANY OF BIOLOGISTS LTD
official_url: http://dx.doi.org/10.1242/dev.147926
oa_status: green
full_text_type: pub
language: eng
primo: open
primo_central: open_green
article_type_text: Article
verified: verified_manual
elements_id: 1297121
doi: 10.1242/dev.147926
lyricists_name: Barriga, Elias Hernan
lyricists_name: Frankel, Paul
lyricists_name: Mayor, Roberto
lyricists_id: EHBAR83
lyricists_id: PFRAN76
lyricists_id: RMAYO52
actors_name: Dewerpe, Marie
actors_id: MDDEW97
actors_role: owner
full_text_status: public
publication: Development
volume: 144
number: 13
pagerange: 2456-2468
pages: 13
issn: 1477-9129
citation:        Bahm, I;    Barriga, EH;    Frolov, A;    Theveneau, E;    Frankel, P;    Mayor, R;      (2017)    PDGF controls contact inhibition of locomotion by regulating N-cadherin during neural crest migration.                   Development , 144  (13)   pp. 2456-2468.    10.1242/dev.147926 <https://doi.org/10.1242/dev.147926>.       Green open access   
 
document_url: https://discovery.ucl.ac.uk/id/eprint/1558498/1/Frankel_2456.full.pdf