Thyroid hormone and retinoic acid interact to regulate zebrafish craniofacial neural crest development

Brenda L. Bohnsack, Alon Kahana*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

58 Scopus citations


Craniofacial and ocular morphogenesis require proper regulation of cranial neural crest migration, proliferation, survival and differentiation. Although alterations in maternal thyroid hormone (TH) are associated with congenital craniofacial anomalies, the role of TH on the neural crest has not been previously described. Using zebrafish, we demonstrate that pharmacologic and genetic alterations in TH signaling disrupt cranial neural crest migration, proliferation, and survival, leading to craniofacial, extraocular muscle, and ocular developmental abnormalities. In the rostral cranial neural crest that gives rise to the periocular mesenchyme and the frontonasal process, retinoic acid (RA) rescued migratory defects induced by decreased TH signaling. In the caudal cranial neural crest, TH and RA had reciprocal effects on anterior and posterior pharyngeal arch development. The interactions between TH and RA signaling were partially mediated by the retinoid X receptor. We conclude that TH regulates both rostral and caudal cranial neural crest. Further, coordinated interactions of TH and RA are required for proper craniofacial and ocular development.

Original languageEnglish (US)
Pages (from-to)300-309
Number of pages10
JournalDevelopmental Biology
Issue number2
StatePublished - Jan 15 2013
Externally publishedYes


  • Craniofacial
  • Eye development
  • Migration
  • Neural crest
  • Pharyngeal arch
  • Pitx2
  • Retinoic acid
  • Retinoid X receptor
  • Thyroid hormone
  • Twist1

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology


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