Expanding Actin Rings Zipper the Mouse Embryo for Blastocyst Formation

BIRO, MATÉ; ALVAREZ, YANINA D.; ZENKER, JENNIFER; BISSIERE, STEPHANIE; GASNIER, MAXIME; PLACHTA, NICOLAS; LIM, HUI YI GRACE; WHITE, MELANIE D.

CELL

CELL PRESS

Año: 2018 vol. 173 p. 1 - 16

0092-8674

Transformation from morula to blastocyst is a defining event of preimplantation embryo development. During this transition, the embryo must establish a paracellular permeability barrier to enable expansion of the blastocyst cavity. Here, using live imaging of mouse embryos, we reveal an actin-zippering mechanism driving this embryo sealing. Preceding blastocyst stage, a cortical F-actin ring assembles at the apical pole of the embryo?s outer cells. The ring structure forms when cortical actin flows encounter a network of polar microtubules that exclude F-actin. Unlike stereotypical actin rings, the actin rings of the mouse embryo are not contractile, but instead, they expand to the cell-cell junctions. Here, they couple to the junctions by recruiting and stabilizing adherens and tight junction components. Coupling of the actin rings triggers localized myosin II accumulation, and it initiates a tension-dependent zippering mechanism along the junctions that is required to seal the embryo for blastocyst formation