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Mol Cell Endocrinol. 2017 Jan 5;439:233-246. doi: 10.1016/j.mce.2016.09.007. Epub 2016 Sep 10.

Implication of thyroid hormone signaling in neural crest cells migration: Evidence from thyroid hormone receptor beta knockdown and NH3 antagonist studies.

Author information

1
Paris-Saclay Institute of Neuroscience, CNRS, Univ. Paris-Sud, Université Paris-Saclay, 91405, Orsay, France. Electronic address: odile.bronchain@u-psud.fr.
2
Paris-Saclay Institute of Neuroscience, CNRS, Univ. Paris-Sud, Université Paris-Saclay, 91405, Orsay, France.
3
Univ Paris Sud, Université Paris Saclay, Centre Universitaire, F-91405, Orsay, France; Institut Curie PSL Research University, Centre Universitaire, F-91405, Orsay, France; UMR 3347 CNRS, U1021 Inserm, Université Paris Saclay, Centre Universitaire, F-91405, Orsay, France.
4
CNRS, Sorbonne Universités, UPMC University Paris 06, UMR8226, Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, Institut de Biologie Physico-Chimique, 75005, Paris, France; UMR 7221 CNRS, Muséum National d'histoire Naturelle, Dépt. Régulation, Développement et Diversité Moléculaire, Sorbonne Universités, 75005, Paris, France.
5
Watchfrog S.A., 1 Rue Pierre Fontaine, 91000, Evry, France; Institute of Systems and Synthetic Biology, CNRS, Université d'Evry Val d'Essonne, Bâtiment 3, Genopole(®) Campus 3, 1, Rue Pierre Fontaine, F-91058, Evry, France.
6
Department of Physiology & Pharmacology, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, L334, Portland, OR, 97239-3098, USA.
7
UMR 7221 CNRS, Muséum National d'histoire Naturelle, Dépt. Régulation, Développement et Diversité Moléculaire, Sorbonne Universités, 75005, Paris, France.
8
Institute of Systems and Synthetic Biology, CNRS, Université d'Evry Val d'Essonne, Bâtiment 3, Genopole(®) Campus 3, 1, Rue Pierre Fontaine, F-91058, Evry, France; Evolution, Génomes, Comportement & Ecologie, CNRS, IRD, Univ. Paris-Sud, Université Paris-Saclay, 91198, Gif-sur-Yvette, France.

Abstract

Thyroid hormones (TH) have been mainly associated with post-embryonic development and adult homeostasis but few studies report direct experimental evidence for TH function at very early phases of embryogenesis. We assessed the outcome of altered TH signaling on early embryogenesis using the amphibian Xenopus as a model system. Precocious exposure to the TH antagonist NH-3 or impaired thyroid receptor beta function led to severe malformations related to neurocristopathies. These include pathologies with a broad spectrum of organ dysplasias arising from defects in embryonic neural crest cell (NCC) development. We identified a specific temporal window of sensitivity that encompasses the emergence of NCCs. Although the initial steps in NCC ontogenesis appeared unaffected, their migration properties were severely compromised both in vivo and in vitro. Our data describe a role for TH signaling in NCCs migration ability and suggest severe consequences of altered TH signaling during early phases of embryonic development.

KEYWORDS:

Embryonic development; NH-3; Neural crest cells migration; THRB knockdown; Thyroid hormone; Xenopus

PMID:
27619407
DOI:
10.1016/j.mce.2016.09.007
[Indexed for MEDLINE]

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