作者: Christina Chatzi , Thomas J. Cunningham , Gregg Duester
DOI: 10.1002/DVDY.23999
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摘要: Background: Retinoic acid (RA) signaling controls patterning and neuronal differentiation within the hindbrain, but forebrain RA function remains controversial. is produced from metabolism of retinol to retinaldehyde by dehydrogenase (RDH), followed (RALDH). Previous studies on Raldh2−/− Raldh3−/− mice demonstrated an requirement for γ-aminobutyric (GABA)ergic dopaminergic in basal ganglia, no was observed during early or subsequent cortical expansion. However, other suggested that patterning, analysis ethylnitrosourea-induced Rdh10 mutants synthesized meninges stimulates Results: We generated Rdh10−/− mouse embryos lack activity head later meninges. defects hindbrain eye signaling, unaffected. Retinaldehyde treatment E7–E9 rescues a cranial skeletal defect, resulting E14.5 lacking meningeal maintaining normal shape Conclusions: demonstrate not while retinaldehyde-rescued show synthesis unnecessary stimulate Developmental Dynamics 242:1056–1065, 2013. © 2013 Wiley Periodicals, Inc.