| Summary: | <p>Abstract</p> <p>Background</p> <p>The zebrafish, <it>Danio rerio</it>, possesses the paralogous genes <it>aplnra </it>and <it>aplnrb </it>that are duplicates of an ancestral orthologue of the human <it>APLNR </it>gene encoding a G-protein coupled receptor that binds the peptide ligand APELIN and is required for normal cardiovascular function. <it>aplnrb </it>is required for migration of cells contributing to heart development in zebrafish embryos. <it>aplnra </it>is transcribed in a complex pattern during early development but its function in embryogenesis is largely unknown.</p> <p>Findings</p> <p>Blockage of translation of <it>aplnra </it>mRNA in zebrafish embryos results in retarded or failed epiboly with the blastoderm apparently disconnected from the nuclei of the yolk syncytial layer. Gastrulation is also defective. Failure of correct tail extension is observed with ectopic structures resembling somites positioned dorsal to the spinal cord.</p> <p>Conclusion</p> <p><it>aplnra</it>, unlike its duplicate <it>aplnrb</it>, is essential for normal epiboly, although this function appears to be independent of signalling activated by zebrafish Apelin. The defects in epiboly caused by loss of <it>aplnra </it>activity appear, at least partially, to be due to a requirement for <it>aplnra </it>activity in the yolk syncytial layer.</p>
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