Expanding Actin Rings Zipper the Mouse Embryo for Blastocyst Formation

JENNIFER ZENKER; MAXIME GASNIER; MELANIE D. WHITE; ALVAREZ, YANINA; HUI YI GRACE LIM

Congreso; Vietnam 2nd meeting when physics meets biology; 2019

Transformationfrom morula to blastocyst is a defining event of preimplantation embryodevelopment. During this transition, the embryo must establish a paracellularpermeability barrier to enable expansion of the blastocyst cavity. Here, usinglive imaging of mouse embryos, we reveal an actin-zippering mechanism drivingthis embryo sealing. Preceding blastocyst stage, a cortical F-actin ringassembles at the apical pole of the embryo?s outer cells. The ring structureforms when cortical actin flows encounter a network of polar microtubules thatexclude F-actin. Unlike stereotypical actin rings, the actin rings of the mouseembryo are not contractile, but instead, they expand to the cell-celljunctions. Here, they couple to the junctions by recruiting and stabilizingadherens and tight junction components. Coupling of the actin rings triggerslocalized myosin II accumulation and it initiates a tension-dependent zipperingmechanism along the junctions that is required to seal the embryo forblastocyst formation.