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Cadherin-dependent filopodia control preimplantation embryo compaction
Juan Carlos Fierro-González1, Melanie D White, Juan Carlos Silva
11] European Molecular Biology Laboratory, Australian Regenerative Medicine Institute, Level 1 Building 75, Monash University, Victoria 3800, Australia [2].
Nature Cell Biology
|November 26, 2013
Summary
Mammalian embryo compaction involves cell elongation, driven by E-cadherin-dependent filopodia. These cell projections are crucial for maintaining cell shape and enabling embryonic development.
Area of Science:
- Developmental biology
- Cell biology
- Morphogenesis
Background:
- Compaction is the initial morphogenetic event in mammalian preimplantation embryos.
- The cellular mechanisms driving cell elongation during compaction remain largely unknown.
Purpose of the Study:
- To elucidate the role of cell shape changes in mammalian embryonic compaction.
- To identify the molecular mechanisms underlying cell elongation during early development.
Main Methods:
- Live imaging of mouse embryos.
- Laser-based cell ablation.
- Molecular disruption of key cellular components.
- Overexpression of specific proteins.
Main Results:
- Cells extend E-cadherin-dependent filopodia onto neighboring cells, facilitating compaction.
- Filopodia extension correlates with cell elongation, and retraction precedes cell division.
- Disruption of filopodia components (E-cadherin, catenins, F-actin, myosin-X) inhibits cell elongation and compaction.
- Overexpression of myosin-X induces premature compaction.
Conclusions:
- Filopodia play a critical role in mammalian preimplantation embryonic compaction.
- Filopodia mediate the cell shape changes essential for forming a compacted embryo.
- This study provides an in vivo model to investigate filopodia functions in mammalian development.
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