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Sonic Hedgehog Signaling Is Required for Cyp26 Expression during Embryonic Development

Journal article
Authors Maha El Shahawy
Claes-Göran Reibring
Kristina Hallberg
C. L. Neben
P. Marangoni
B. D. Harfe
O. D. Klein
Anders Linde
Amel Gritli Linde
Published in International Journal of Molecular Sciences
Volume 20
Issue 9
ISSN 1422-0067
Publication year 2019
Published at Institute of Odontology
Language en
Keywords Cyp26 enzymes, congenital anomalies, CRE, LoxP, hedgehog signaling, mouse models, retinoic acid, retinoic acid synthesis, apical ectodermal ridge, neural crest cells, all-trans, vitamin-a, limb bud, retinaldehyde dehydrogenase, secondary, palate, receptor-gamma, cleft-lip
Subject categories Cell and Molecular Biology


Deciphering how signaling pathways interact during development is necessary for understanding the etiopathogenesis of congenital malformations and disease. In several embryonic structures, components of the Hedgehog and retinoic acid pathways, two potent players in development and disease are expressed and operate in the same or adjacent tissues and cells. Yet whether and, if so, how these pathways interact during organogenesis is, to a large extent, unclear. Using genetic and experimental approaches in the mouse, we show that during development of ontogenetically different organs, including the tail, genital tubercle, and secondary palate, Sonic hedgehog (SHH) loss-of-function causes anomalies phenocopying those induced by enhanced retinoic acid signaling and that SHH is required to prevent supraphysiological activation of retinoic signaling through maintenance and reinforcement of expression of the Cyp26 genes. Furthermore, in other tissues and organs, disruptions of the Hedgehog or the retinoic acid pathways during development generate similar phenotypes. These findings reveal that rigidly calibrated Hedgehog and retinoic acid activities are required for normal organogenesis and tissue patterning.

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