Dataset Information

Expression profiling of control vs. ta/tbx16 double knockdown zebrafish embryos at shield and 90% epiboly

ABSTRACT: Identification of genes downstream of ta/tbx16 in zebrafish embryos, and identification of direct targets by reference to Ta and Tbx16 ChIP-seq data

ORGANISM(S): Danio rerio

PROVIDER: GSE84611 | GEO | 2017/06/11

SECONDARY ACCESSION(S): PRJNA330633

REPOSITORIES: GEO

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Project description:Transcriptional profiling of 50% epiboly zebrafish embryos comparing wildtype (control) to Aplnra/b morpholino injected embryos. Goal was to determine any gene expression changes in embryos deficient for the Apelin receptor. Publication summary: The Apelin receptor (Aplnr) has been shown to be essential for proper cardiac progenitor migration during gastrulation. Loss of the Aplnr results in a delay in the ingression of lateral marginal cells and the complete absence of the heart and early cardiac gene expression. How the Aplnr is required at a molecular level for cardiac progenitor migration remains completely unknown. We present evidence to suggest that the Aplnr enhances Nodal signaling to initiate the migration program at the correct time in development. Apelin receptor loss of function embryos exhibit a reduction in a wide range of Nodal target genes while activation of the receptor is capable of boosting their expression. Furthermore, Aplnr deficient embryos are exquisitely sensitive to Nodal receptor inhibitors. In order to directly interrogate the functional consequence of reduced Nodal signaling in the Aplnr cardiac phenotype, we raised the level of Nodal activity in aplnr mutants and found that this was able to provide a near complete rescue. We next sought to determine a mechanism by which lower Nodal signaling levels could translate into a delay in migration. Remarkably, we observe a delay in the expression of mesp family members in Aplnr loss of function embryos at the beginning of gastrulation. The mesp family has previously been implicated in mesodermal migration and we show that they are downstream targets of Nodal. We propose that in the absence of the Aplnr the appropriate Nodal threshold required to initiate the downstream cardiac progenitor “specification/migration” program requires a longer length of time to be attained. This translates into a delay in migration and consequently cardiac progenitors are not capable of reaching their final destination. In this study we demonstrate how the fine tuning of a key signaling pathway is critical for the proper development of the early embryo.

Dataset Information

Expression profiling of control vs. ta/tbx16 double knockdown zebrafish embryos at shield and 90% epiboly

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