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 a non-cell autonomous activity of Zic1 and implicate retinoic acid (RA) signaling 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 program in neighboring cells.
Highlights
All cranial placode progenitors arise from a common precursor field anterior to the neural plate, the pre-placodal region (PPR)
Among the targets regulated by Zic[1], we found a number of genes involved in the synthesis and metabolism of retinoic acid (RA) including lipocalin-type prostaglandin D2 synthase (LPGDS), retinaldehyde dehydrogenase 2 (RALDH2), two members of the cytochrome P450 enzyme family (Cyp26a and Cyp26c) and a cellular RA-binding protein 2 (Crabp2) signifying the importance of this signalling pathway in placode formation
We have identified several genes activated by Zic[1] that are involved in RA metabolism and function
Summary
All cranial placode progenitors arise from a common precursor field anterior to the neural plate, the pre-placodal region (PPR). Cranial sensory placodes are thickenings of the embryonic head ectoderm that give rise to the specialized paired sense organs and sensory cranial ganglia While they produce very diverse cell types such as sensory neurons, lens fibres and hormone-secreting cells[1,2,3], all placode progenitors arise from a common precursor field that borders the anterior neural plate known as the pre-placodal region (PPR). Among the targets regulated by Zic[1], we found a number of genes involved in the synthesis and metabolism of retinoic acid (RA) including lipocalin-type prostaglandin D2 synthase (LPGDS), retinaldehyde dehydrogenase 2 (RALDH2), two members of the cytochrome P450 enzyme family (Cyp26a and Cyp26c) and a cellular RA-binding protein 2 (Crabp2) signifying the importance of this signalling pathway in placode formation. We present evidence that Zic[1] regulates placode progenitor formation non-cell autonomously by controlling RA production and transport at the anterior neural plate
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