The endoderm indirectly influences morphogenetic movements of the zebrafish head kidney through the posterior cardinal vein and VegfC.

Integration of blood vessels and organ primordia determines organ shape and function. The head kidney in the zebrafish interacts with the dorsal aorta (DA) and the posterior cardinal vein (PCV) to achieve glomerular filtration and definitive hematopoiesis, respectively. How the head kidney co-develops with both the axial artery and vein remains unclear. We found that in endodermless sox32-deficient embryos, the head kidney associated with the PCV but not the DA. Disrupted convergent migration of the PCV and the head kidney in sox32-deficient embryos was rescued in a highly coordinated fashion through the restoration of endodermal cells. Moreover, grafted endodermal cells abutted the host PCV endothelium in the transplantation assay. Interestingly, the severely-disrupted head kidney convergence in the sox32-deficient embryo was suppressed by both the cloche mutation and the knockdown of endothelial genes, indicating that an interaction between the endoderm and the PCV restricts the migration of the head kidney. Furthermore, knockdown of either vegfC or its receptor vegfr3 suppressed the head kidney convergence defect in endodermless embryos and perturbed the head kidney-PCV association in wild-type embryos. Our findings thus underscore a role for PCV and VegfC in patterning the head kidney prior to organ assembly and function.

Arterial and venous vessels are required for modulating developmental relocalization and laterality of the interrenal tissue in zebrafish.

During zebrafish embryogenesis, the endothelium signals to emergent bilateral interrenal primordia to converge toward the midline, yet the merged interrenal tissue has been found to be situated lateral to the midline. We show in this study that bilateral interrenal tissue clusters fused at the central midline, before relocating laterally to be juxtaposed between the dorsal aorta and the posterior cardinal vein. In ets1b morphants where the midtrunk vasculature failed to assemble, various degrees of interrenal fusion defects were displayed, and the interrenal laterality was lost. As either arterial or venous endothelium was specifically reduced, the interrenal tissue was defective in its relocalization and laterality, yet remained closely associated with the malformed vasculature. Our results showed evidence to support that assembly of the axial artery and vein, and its resulting vascular topology at the midtrunk, is required for patterning relocalization and laterality of the interrenal tissue after the initial medial fusion.