Journal
DEVELOPMENTAL CELL
Volume 34, Issue 4, Pages 435-447Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2015.07.004
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Funding
- Multi-modal Australian ScienceS Imaging and Visualisation Environment (MASSIVE)
- Australian Research Council [DP120104594, DE120100794]
- National Health and Medical Research Council [APP1022721, APP1052171, APP1062263]
- Viertel Foundation Medical Research Fellowship
- Monash University
- UK Medical Research Council [G0802057]
- Wenner-Gren Foundations
- Swedish Society for Medical Research
- A*STAR [1430700132]
- MRC [G0802057] Funding Source: UKRI
- Medical Research Council [G0802057] Funding Source: researchfish
- Australian Research Council [DE120100794] Funding Source: Australian Research Council
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Every cell in our body originates from the pluripotent inner mass of the embryo, yet it is unknown how biomechanical forces allocate inner cells in vivo. Here we discover subcellular heterogeneities in tensile forces, generated by actomyosin cortical networks, which drive apical constriction to position the first inner cells of living mouse embryos. Myosin II accumulates specifically around constricting cells, and its disruption dysregulates constriction and cell fate. Laser ablations of actomyosin networks reveal that constricting cells have higher cortical tension, generate tension anisotropies and morphological changes in adjacent regions of neighboring cells, and require their neighbors to coordinate their own changes in shape. Thus, tensile forces determine the first spatial segregation of cells during mammalian development. We propose that, unlike more cohesive tissues, the early embryo dissipates tensile forces required by constricting cells via their neighbors, thereby allowing confined cell repositioning without jeopardizing global architecture.
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