Talk:Vision - Extraocular Muscle Development: Difference between revisions
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===Thyroid hormone and retinoic acid interact to regulate zebrafish craniofacial neural crest development=== | |||
Dev Biol. 2013 Jan 15;373(2):300-9. doi: 10.1016/j.ydbio.2012.11.005. Epub 2012 Nov 17. | |||
Bohnsack BL, Kahana A. | |||
Source | |||
Department of Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor, MI, USA. | |||
Abstract | |||
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. | |||
Copyright © 2012 Elsevier Inc. All rights reserved. | |||
PMID 23165295 |
Revision as of 19:04, 19 May 2013
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Cite this page: Hill, M.A. (2024, June 26) Embryology Vision - Extraocular Muscle Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Vision_-_Extraocular_Muscle_Development |
2013
Thyroid hormone and retinoic acid interact to regulate zebrafish craniofacial neural crest development
Dev Biol. 2013 Jan 15;373(2):300-9. doi: 10.1016/j.ydbio.2012.11.005. Epub 2012 Nov 17.
Bohnsack BL, Kahana A. Source Department of Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor, MI, USA.
Abstract
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. Copyright © 2012 Elsevier Inc. All rights reserved.
PMID 23165295