Please use this identifier to cite or link to this item: https://doi.org/10.7554/eLife.13758
Title: The Apelin receptor enhances Nodal/TGF? signaling to ensure proper cardiac development
Authors: Deshwar, A.R
Chng, S.C
Ho, L
Reversade, B 
Scott, I.C
Keywords: apelin receptor
transforming growth factor beta
apelin receptor, zebrafish
G protein coupled receptor
protein Nodal
transforming growth factor beta
zebrafish protein
animal experiment
Article
embryo
gastrulation
gene expression
genotype
heart development
in situ hybridization
luciferase assay
microarray analysis
nonhuman
phenotype
polymerase chain reaction
protein expression
signal transduction
upregulation
zebra fish
animal
embryology
heart
metabolism
signal transduction
Animals
Heart
Nodal Protein
Receptors, G-Protein-Coupled
Signal Transduction
Transforming Growth Factor beta
Zebrafish
Zebrafish Proteins
Issue Date: 2016
Citation: Deshwar, A.R, Chng, S.C, Ho, L, Reversade, B, Scott, I.C (2016). The Apelin receptor enhances Nodal/TGF? signaling to ensure proper cardiac development. eLife 5 (42461) : e13758. ScholarBank@NUS Repository. https://doi.org/10.7554/eLife.13758
Rights: Attribution 4.0 International
Abstract: The Apelin receptor (Aplnr) is essential for heart development, controlling the early migration of cardiac progenitors. Here we demonstrate that in zebrafish Aplnr modulates Nodal/TGF? signaling, a key pathway essential for mesendoderm induction and migration. Loss of Aplnr function leads to a reduction in Nodal target gene expression whereas activation of Aplnr by a non-peptide agonist increases the expression of these same targets. Furthermore, loss of Aplnr results in a delay in the expression of the cardiogenic transcription factors mespaa/ab. Elevating Nodal levels in aplnra/b morphant and double mutant embryos is sufficient to rescue cardiac differentiation defects. We demonstrate that loss of Aplnr attenuates the activity of a point source of Nodal ligands Squint and Cyclops in a non-cell autonomous manner. Our results favour a model in which Aplnr is required to fine-tune Nodal output, acting as a specific rheostat for the Nodal/TGF? pathway during the earliest stages of cardiogenesis. © Deshwar et al.
Source Title: eLife
URI: https://scholarbank.nus.edu.sg/handle/10635/178923
ISSN: 2050084X
DOI: 10.7554/eLife.13758
Rights: Attribution 4.0 International
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