Spatiotemporal regulation of actomyosin directs morphogenesis of blood vessel lumens

What is it about?

This work delves into the mechanisms by which the scaffolding protein Rasip1 works via different GTPase pathways to regulate the activity of actomyosin at different times and places to change endothelial cell shape and adhesion. These coordinated cellular process allows endothelial cells to remove junctions from the center of primitive vascular cords, thereby allowing the apical/luminal membrane to be cleared and lumens to open in a continuous manner. This is then followed by inflow of blood into these newly formed vascular tubes. Upon new hemodynamic forces caused by blood flow, the apical surface of blood reacts by activating NMII tension. This is then released by Rasip1 suppression of RhoA signaling via the GTPase activating protein Arhgap29. This results in endothelial relaxation, which allows vascular lumens to expand as vessels grow in the embryo.

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Why is it important?

These findings are significant because they underscore how signaling molecules can act in different places and times within the endothelial cell itself. Formation of blood vessel lumens is a step-wise process, which coordinates a number of different events in a highly regulated manner.