Abstract
Essential cellular components of the paired sensory organs of the vertebrate head are derived from transient thickenings of embryonic ectoderm known as cranial placodes. The epibranchial (EB) placodes give rise to sensory neurons of the EB ganglia that are responsible for relaying visceral sensations form the periphery to the central nervous system. Development of EB placodes and subsequent formation of EB ganglia is a multistep process regulated by various extrinsic factors, including fibroblast growth factors (Fgfs). We discovered that two Fgf ligands, Fgf3 and Fgf10a, cooperate to promote EB placode development. Whereas EB placodes are induced in the absence of Fgf3 and Fgf10a, they fail to express placode specific markers Pax2a and Sox3. Expression analysis and mosaic rescue experiments demonstrate that Fgf3 signal is derived from the endoderm, whereas Fgf10a is emitted from the lateral line system and the otic placode. Further analyses revealed that Fgf3 and Fgf10a activities are not required for cell proliferation or survival, but are required for placodal cells to undergo neurogenesis. Based on these data, we conclude that a combined loss of these Fgf factors results in a failure of the EB placode precursors to initiate a transcriptional program needed for maturation and subsequent neurogenesis. These findings highlight the importance and complexity of reiterated Fgf signaling during cranial placode formation and subsequent sensory organ development.
Highlights
In the developing vertebrate head, essential cellular components of the paired sensory organs originate from anatomically distinct structures consisting of neurogenic epithelium called cranial placodes
We find that injection of fgf10a-morpholino oligonucleotides (MO) into fgf3-/- mutant embryos resulted in loss of the facial placode, a nearly complete loss of the glossopharyngeal and vagal placodes at 24 hpf, and an absence of the respective ganglia at 72 hpf
We have previously demonstrated that fibroblast growth factors (Fgfs) activity is required for EB placode development during the second half of segmentation [12,17]
Summary
In the developing vertebrate head, essential cellular components of the paired sensory organs originate from anatomically distinct structures consisting of neurogenic epithelium called cranial placodes. Combined inactivation of Fgf3 and Fgf10a resulted in a complete loss Pax2a expression in the facial placode, and a near complete loss of Pax2a expression in the glossopharyngeal/vagal placode at 24 hpf (Figure 2F,G). In addition to Pax2a, we observed a loss of sox3 expression in Fgf3+10a deficient embryos at 24 hpf (Figure S2C,D).
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