Abstract

BackgroundAlthough retinoic acid (RA) signaling plays a crucial role in the body patterning of chordates, its function in non-chordate invertebrates, other than its mediation of environmental cues triggering metamorphosis in cnidarians, is largely unknown. We investigated the role of RA signaling in the metamorphosis of starfish (Echinodermata).ResultsWe found that exogenous RA treatment induced metamorphosis in starfish larvae. In contrast, inhibitors of RA synthesis and RA receptors suppressed metamorphosis triggered by attachment to a substrate. Gene expressions of the RA signaling component were detected in competent larvae.ConclusionsThis study provides insight into the ancestral function of RA signaling, which is conserved in the metamorphosis of cnidarians and starfish.

Highlights

  • Retinoic acid (RA) signaling plays a crucial role in the body patterning of chordates, its function in non-chordate invertebrates, other than its mediation of environmental cues triggering metamorphosis in cnidarians, is largely unknown

  • retinoid x receptor (RXR) was identified in various metazoan taxa including cnidarian, arthropod, and nematode [4], retinal dehydrogenase (Raldh) and retinoic acid receptor (RAR), as well as cytochrome P450 26 (CYP26), which degrades retinoic acid (RA), had been described only in chordates, and RA signaling was thought to be specific to chordates, and the acquisition of the gene families for RA signaling was thought to be a key step in the evolution of the chordate body plan [3]

  • Competence for metamorphosis was acquired around 8 dpf in P. pectinifera As in other echinoderm species, the transition from larval form to adult form proceeds via multiple steps in starfish

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Summary

Introduction

Retinoic acid (RA) signaling plays a crucial role in the body patterning of chordates, its function in non-chordate invertebrates, other than its mediation of environmental cues triggering metamorphosis in cnidarians, is largely unknown. Following additional genomic surveys of other invertebrates, the origin of RA signaling was pushed back to the common ancestor of metazoans [6, 7]. Despite these genomic surveys, the function of RA signaling in non-chordate deuterostomes remains largely unknown, other than the observation of pseudopodial cable growth on micromere-delivered cells from Hemicentrotus pulcherrimus after RA treatment [8]. Marlétaz et al suggested that the promoter region of sea urchin Hox genes had an RA response element [3], no additional evidence of the effect of RA on Hox gene expression has been reported

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