Antagonistic interactions among Plexins regulate the timing of intersegmental vessel formation

Area of Science:

• Developmental biology
• Vascular biology
• Cell signaling

Background:

• Angioblasts are embryonic endothelial cell precursors migrating via environmental cues.
• Semaphorins are implicated in angioblast behavior, but in vivo roles are unclear.

Purpose of the Study:

• To investigate the in vivo roles of semaphorin3e (Sema3e) and its receptors, PlexinB2 (PlxnB2) and PlexinD1 (PlxnD1), in zebrafish angioblast migration and intersegmental vessel (ISV) formation.

Main Methods:

• Analysis of zebrafish sema3e, plxnB2, and plexinD1 (obd) mutants and morphants.
• Transplant experiments to assess autonomous and non-autonomous functions.
• Phenotypic analysis of ISV sprouting and angioblast migration.

Main Results:

• Loss of Sema3e delays angioblast exit from the dorsal aorta and ISV formation.
• Loss of PlxnB2 phenocopies sema3e loss, while loss of PlxnD1 leads to precocious ISV sprouting.
• Sema3e/PlxnB2 and PlxnD1 antagonize each other to regulate ISV sprouting timing.

Conclusions:

• Multiple semaphorin-plexin interactions, including Sema3e/PlxnB2 and PlxnD1, are crucial for controlling angioblast sprouting behavior and ISV development in vivo.
• PlxnB2 acts cell autonomously in endothelial cells during ISV formation.