scholarly journals Retinaldehyde dehydrogenase 2 (RALDH2)-mediated retinoic acid synthesis regulates early mouse embryonic forebrain development by controlling FGF and sonic hedgehog signaling

Development ◽  
2005 ◽  
Vol 133 (2) ◽  
pp. 351-361 ◽  
Author(s):  
V. Ribes
Keyword(s):  
Retinoic Acid ◽  
Sonic Hedgehog ◽  
Hedgehog Signaling ◽  
Acid Synthesis ◽  
Sonic Hedgehog Signaling ◽  
Forebrain Development ◽  
Retinaldehyde Dehydrogenase ◽  
Early Mouse

scholarly journals Hmx4 regulates Sonic hedgehog signaling through control of retinoic acid synthesis during forebrain patterning

2011 ◽  
Vol 355 (1) ◽  
pp. 55-64 ◽  
Author(s):  
Patricia A. Gongal ◽  
Lindsey D. March ◽  
Vanessa L. Holly ◽  
Laura M. Pillay ◽  
Karyn M. Berry-Wynne ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Sonic Hedgehog ◽  
Hedgehog Signaling ◽  
Acid Synthesis ◽  
Sonic Hedgehog Signaling

scholarly journals Sonic Hedgehog Signaling Is Required for Cyp26 Expression during Embryonic Development

2019 ◽  
Vol 20 (9) ◽  
pp. 2275 ◽  
Author(s):  
Maha El Shahawy ◽  
Claes-Göran Reibring ◽  
Kristina Hallberg ◽  
Cynthia L. Neben ◽  
Pauline Marangoni ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Sonic Hedgehog ◽  
Congenital Malformations ◽  
Hedgehog Signaling ◽  
Retinoic Acid Signaling ◽  
Loss Of Function ◽  
Sonic Hedgehog Signaling ◽  
Secondary Palate ◽  
Experimental Approaches ◽  
Genital Tubercle

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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