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• W3128449495 abstract "All paired sensory organs arise from a common precursor domain called the pre-placodal region (PPR). In Xenopus, Zic1 non-cell autonomously regulates PPR formation by activating retinoic acid (RA) production. Here, we have identified two Zic1 targets, the RA catabolizing enzyme Cyp26c1 and the transcription factor Pitx2c, expressed in the vicinity of the PPR as being crucially required for maintaining low RA levels in a spatially restricted, PPR-adjacent domain. Morpholino- or CRISPR/Cas9-mediated Cyp26c1 knockdown abrogated PPR gene expression, yielding defective cranial placodes. Direct measurement of RA levels revealed that this is mediated by a mechanism involving excess RA accumulation. Furthermore, we show that pitx2c is activated by RA and required for Cyp26c1 expression in a domain-specific manner through induction of FGF8. We propose that Zic1 anteriorly establishes a program of RA containment and regulation through activation of Cyp26c1 and Pitx2c that cooperates to promote PPR specification in a spatially restricted domain." @default.
• W3128449495 created "2021-02-15" @default.
• W3128449495 creator A5010040572 @default.
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• W3128449495 date "2021-02-15" @default.
• W3128449495 modified "2023-10-14" @default.
• W3128449495 title "Retinoic acid production, regulation and containment through Zic1, Pitx2c and Cyp26c1 control cranial placode specification" @default.
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• W3128449495 doi "https://doi.org/10.1242/dev.193227" @default.
• W3128449495 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7903997" @default.
• W3128449495 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33531433" @default.
• W3128449495 hasPublicationYear "2021" @default.
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