RT Journal Article
SR Electronic
T1 Mechanics of human embryo compaction
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2022.01.09.475429
DO 10.1101/2022.01.09.475429
A1 Julie Firmin
A1 Nicolas Ecker
A1 Diane Rivet Danon
A1 Virginie Barraud Lange
A1 Hervé Turlier
A1 Catherine Patrat
A1 Jean-Léon Maître
YR 2022
UL http://biorxiv.org/content/early/2022/01/11/2022.01.09.475429.abstract
AB The shaping of the human embryo begins with compaction, during which cells come into close contact and form a tighter structure1,2. Assisted reproductive technology (ART) studies suggest that human embryos fail compaction primarily because of defective adhesion3,4. Based on our current understanding of animal morphogenesis5,6, other morphogenetic engines, such as cell contractility, could be involved in shaping the human embryo. However, the molecular, cellular and physical mechanisms driving human embryo morphogenesis remain uncharacterized. Using micropipette aspiration on human embryos donated to research, we have mapped cell surface tensions during compaction. This reveals a 4-fold increase of tension at the cellmedium interface while cell-cell contacts keep a steady tension. Comparison between human and mouse reveals qualitatively similar but quantitively different mechanical strategies, with human embryos being mechanically least efficient. Inhibition of cell contractility and cell-cell adhesion in human embryos reveal that only contractility controls the surface tension responsible for compaction. Interestingly, if both cellular processes are required for compaction, they exhibit distinct mechanical signatures when faulty. Analyzing the mechanical signature of naturally failing embryos, we find evidence that non-compacting embryos or partially compacting embryos with excluded cells have defective contractility. Together, our study reveals that an evolutionarily conserved increase in cell contractility is required to generate the forces driving the first morphogenetic movement shaping the human body.Competing Interest StatementThe authors have declared no competing interest.