Zic1 controls placode progenitor formation non-cell autonomously by regulating retinoic acid production and transport

Maria Belen Jaurena, Hugo Juraver-Geslin, Arun Devotta, Jean-Pierre Saint-Jeannet

Research output: Contribution to journalArticle

Abstract

All cranial placode progenitors arise from a common precursor field anterior to the neural plate, the pre-placodal region (PPR). We showed that transcription factor Zic1, expressed at the anterior neural plate, is necessary and sufficient to promote placode fate. Here we reveal the non-cell autonomous activity of Zic1 and implicate retinoic acid (RA) signalling as a key player in cranial placode progenitor specification. In a screen for genes activated by Zic1, we identify several factors involved in RA metabolism and function. Among them we show that retinaldehyde dehydrogenase 2 (RALDH2) and lipocalin-type prostaglandin D2 synthase (LPGDS), which, respectively, regulate the synthesis and transport of RA, directly participate in the establishment of the PPR. We propose that RALDH2 and LPGDS induction by Zic1 at the anterior neural plate allows for the localized production and transport of RA, which in turn activates a cranial placode developmental programme in neighbouring cells.

Original languageEnglish (US)
Article number7476
JournalNature Communications
Volume6
DOIs
StatePublished - Jun 23 2015

Fingerprint

prostaglandin R2 D-isomerase
Tretinoin
Neural Plate
prostaglandins
Retinaldehyde
Lipocalins
acids
dehydrogenases
Oxidoreductases
metabolism
Metabolism
genes
specifications
induction
Transcription Factors
Genes
Specifications
synthesis
cells
Lipocalin-2

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Chemistry(all)
  • Physics and Astronomy(all)

Cite this

Zic1 controls placode progenitor formation non-cell autonomously by regulating retinoic acid production and transport. / Jaurena, Maria Belen; Juraver-Geslin, Hugo; Devotta, Arun; Saint-Jeannet, Jean-Pierre.

In: Nature Communications, Vol. 6, 7476, 23.06.2015.

Research output: Contribution to journalArticle

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