The E-cadherin/AmotL2 complex organizes actin filaments required for epithelial hexagonal packing and blastocyst hatching

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Hildebrand , S , Hultin , S , Subramani , A , Petropoulos , S , Zhang , Y , Cao , X , Mpindi , J , Kallioniemi , O , Johansson , S , Majumdar , A , Lanner , F & Holmgren , L 2017 , ' The E-cadherin/AmotL2 complex organizes actin filaments required for epithelial hexagonal packing and blastocyst hatching ' , Scientific Reports , vol. 7 , 9540 . https://doi.org/10.1038/s41598-017-10102-w

Title: The E-cadherin/AmotL2 complex organizes actin filaments required for epithelial hexagonal packing and blastocyst hatching
Author: Hildebrand, Sebastian; Hultin, Sara; Subramani, Aravindh; Petropoulos, Sophie; Zhang, Yuanyuan; Cao, Xiaofang; Mpindi, John; Kallioniemi, Olli; Johansson, Staffan; Majumdar, Arindam; Lanner, Fredrik; Holmgren, Lars
Contributor: University of Helsinki, Institute for Molecular Medicine Finland
University of Helsinki, Institute for Molecular Medicine Finland
Date: 2017-08-25
Language: eng
Number of pages: 17
Belongs to series: Scientific Reports
ISSN: 2045-2322
URI: http://hdl.handle.net/10138/224338
Abstract: Epithelial cells connect via cell-cell junctions to form sheets of cells with separate cellular compartments. These cellular connections are essential for the generation of cellular forms and shapes consistent with organ function. Tissue modulation is dependent on the fine-tuning of mechanical forces that are transmitted in part through the actin connection to E-cadherin as well as other components in the adherens junctions. In this report we show that p100 amotL2 forms a complex with E-cadherin that associates with radial actin filaments connecting cells over multiple layers. Genetic inactivation or depletion of amotL2 in epithelial cells in vitro or zebrafish and mouse in vivo, resulted in the loss of contractile actin filaments and perturbed epithelial packing geometry. We further showed that AMOTL2 mRNA and protein was expressed in the trophectoderm of human and mouse blastocysts. Genetic inactivation of amotL2 did not affect cellular differentiation but blocked hatching of the blastocysts from the zona pellucida. These results were mimicked by treatment with the myosin II inhibitor blebbistatin. We propose that the tension generated by the E-cadherin/AmotL2/actin filaments plays a crucial role in developmental processes such as epithelial geometrical packing as well as generation of forces required for blastocyst hatching.
Subject: CELL-CELL ADHESION
ENDOTHELIAL-CELLS
ADHERENS JUNCTIONS
MOUSE BLASTOCYSTS
FAMILY PROTEINS
E-CADHERIN
ANGIOMOTIN
POLARITY
EMBRYO
MATRIX
3111 Biomedicine
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