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

Odile J. Bronchain, Albert Chesneau, Anne Hélène Monsoro-Burq, Pascale Jolivet, Elodie Paillard, Thomas S. Scanlan, Barbara A. Demeneix, Laurent M. Sachs, Nicolas Pollet

Research output: Contribution to journalArticle

12 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)233-246
Number of pages14
JournalMolecular and Cellular Endocrinology
StatePublished - Jan 5 2017



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

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

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