Nociceptin receptor-mediated Ca2+ channel inhibition and its desensitization in NG108-15 cells

We focus here upon regulation by the notochord of myocardial cell fate in zebrafish. Myocardial precursors, defined by lineage tracing in the living embryo, are in the lateral plate mesoderm adjacent to the notochord-prechordal plate junction. Interestingly, the anterior end of the notochord corresponds to the posterior extent of the heart progenitor field, defined by this lineage analysis. This suggested that the notochord might suppress, or the prechordal plate might enhance, the cardiogenic fate. Nkx2.5 expression is, in the zebrafish embryo, closely correlated with the position of myocardial precursors, which reside adjacent to the notochord-prechordal plate junction. This expression, however, is extinguished in the region posterior to this junction, a region normally not contributing cells to the heart. Laser ablation of the notochord tip between the 4-somite and 12-somite stage causes posterior expansion of the Nkx2. 5-expressing region. The ntl mutation of the notochord is associated with posterior extension of Nkx2.5 expression. Lineage tracking, by laser activation of caged fluoresceinated dextran, confirms that, normally, lateral plate cells next to the notochord do not contribute progeny to the heart. After anterior notochord ablation, these cells are redirected to a heart cell fate. These data suggest that the anterior notochord delimits the posterior extent of the heart field by suppressing the heart cell fate.