Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 439, Issue C, Pages 233-246Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2016.09.007
Keywords
Thyroid hormone; Neural crest cells migration; Embryonic development; Xenopus; NH-3; THRB knockdown
Categories
Funding
- Centre National de la Recherche Scientifique
- Museum National d'Histoire Naturelle
- European Coordinated Action X-OMICS
- FP6 [LSHM-CT-2005-018652, ANR-06-BLAN-0232-01]
- Conseil General de I'Essonne and Genopole ATIGE grant
- CERFAP facility of Genopole
- Association pour la Recherche Contre le Cancer (ARC) [SFI20101201882]
- Fondation pour la recherche Medicale [DEQ20150331733]
- Agence Nationale de la Recherche (ANR-Blanc - SVSE2 -CRESTNET) [ANR-15-CE13-0012-01-CRESTNETMETABO]
Ask authors/readers for more resources
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. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available