FGF and retinoic acid activity gradients control the timing of neural crest cell emigration in the trunk. / Martinez-Morales, Patricia L.; Diez del Corral, Ruth; Olivera-Martinez, Isabel; Quiroga, Alejandra C.; Das, Raman M.; Barbas, Julio A.; Storey, Kate G.; Morales, Aixa V.
In: Journal of Cell Biology, Vol. 194, No. 3, 2011, p. 489-503.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - FGF and retinoic acid activity gradients control the timing of neural crest cell emigration in the trunk
A1 - Martinez-Morales,Patricia L.
A1 - Diez del Corral,Ruth
A1 - Olivera-Martinez,Isabel
A1 - Quiroga,Alejandra C.
A1 - Das,Raman M.
A1 - Barbas,Julio A.
A1 - Storey,Kate G.
A1 - Morales,Aixa V.
AU - Martinez-Morales,Patricia L.
AU - Diez del Corral,Ruth
AU - Olivera-Martinez,Isabel
AU - Quiroga,Alejandra C.
AU - Das,Raman M.
AU - Barbas,Julio A.
AU - Storey,Kate G.
AU - Morales,Aixa V.
PY - 2011
Y1 - 2011
N2 - <p>Coordination between functionally related adjacent tissues is essential during development. For example, formation of trunk neural crest cells (NCCs) is highly influenced by the adjacent mesoderm, but the molecular mechanism involved is not well understood. As part of this mechanism, fibroblast growth factor (FGF) and retinoic acid (RA) mesodermal gradients control the onset of neurogenesis in the extending neural tube. In this paper, using gain-and loss-of-function experiments, we show that caudal FGF signaling prevents premature specification of NCCs and, consequently, premature epithelial-mesenchymal transition (EMT) to allow cell emigration. In contrast, rostrally generated RA promotes EMT of NCCs at somitic levels. Furthermore, we show that FGF and RA signaling control EMT in part through the modulation of elements of the bone morphogenetic protein and Wnt signaling pathways. These data establish a clear role for opposition of FGF and RA signaling in control of the timing of NCC EMT and emigration and, consequently, co-ordination of the development of the central and peripheral nervous system during vertebrate trunk elongation.</p> <p><strong>© 2011 Martínez-Morales et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/)</strong></p>
AB - <p>Coordination between functionally related adjacent tissues is essential during development. For example, formation of trunk neural crest cells (NCCs) is highly influenced by the adjacent mesoderm, but the molecular mechanism involved is not well understood. As part of this mechanism, fibroblast growth factor (FGF) and retinoic acid (RA) mesodermal gradients control the onset of neurogenesis in the extending neural tube. In this paper, using gain-and loss-of-function experiments, we show that caudal FGF signaling prevents premature specification of NCCs and, consequently, premature epithelial-mesenchymal transition (EMT) to allow cell emigration. In contrast, rostrally generated RA promotes EMT of NCCs at somitic levels. Furthermore, we show that FGF and RA signaling control EMT in part through the modulation of elements of the bone morphogenetic protein and Wnt signaling pathways. These data establish a clear role for opposition of FGF and RA signaling in control of the timing of NCC EMT and emigration and, consequently, co-ordination of the development of the central and peripheral nervous system during vertebrate trunk elongation.</p> <p><strong>© 2011 Martínez-Morales et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/)</strong></p>
KW - Epithelial mesenchymal transition
KW - Transcription factor FoxD3
KW - Tyrosine kinase domain
KW - Vertebrate body axis
KW - Neuronal differentiation
KW - Signaling controls
KW - Paraxial mesoderm
KW - Fate restrictions
KW - Opposing FGF
KW - Chick embryo
U2 - 10.1083/jcb.201011077
DO - 10.1083/jcb.201011077
M1 - Article
JO - Journal of Cell Biology
JF - Journal of Cell Biology
SN - 0021-9525
IS - 3
VL - 194
SP - 489
EP - 503
ER -