PUBLICATION

Fluidization-mediated tissue spreading by mitotic cell rounding and non-canonical Wnt signalling

Authors
Petridou, N.I., Grigolon, S., Salbreux, G., Hannezo, E., Heisenberg, C.P.
ID
ZDB-PUB-181219-6
Date
2018
Source
Nature cell biology   21(2): 169-178 (Journal)
Registered Authors
Heisenberg, Carl-Philipp
Keywords
none
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Biomechanical Phenomena
  • Blastoderm/cytology
  • Blastoderm/embryology*
  • Cell Communication/physiology
  • Cell Division
  • Cell Movement/physiology
  • Elasticity
  • Embryo, Nonmammalian/cytology
  • Embryo, Nonmammalian/embryology
  • Mitosis/physiology
  • Morphogenesis*
  • Viscosity
  • Wnt Signaling Pathway/physiology*
  • Zebrafish/embryology*
  • Zebrafish/genetics
PubMed
30559456 Full text @ Nat. Cell Biol.
Abstract
Tissue morphogenesis is driven by mechanical forces that elicit changes in cell size, shape and motion. The extent by which forces deform tissues critically depends on the rheological properties of the recipient tissue. Yet, whether and how dynamic changes in tissue rheology affect tissue morphogenesis and how they are regulated within the developing organism remain unclear. Here, we show that blastoderm spreading at the onset of zebrafish morphogenesis relies on a rapid, pronounced and spatially patterned tissue fluidization. Blastoderm fluidization is temporally controlled by mitotic cell rounding-dependent cell-cell contact disassembly during the last rounds of cell cleavages. Moreover, fluidization is spatially restricted to the central blastoderm by local activation of non-canonical Wnt signalling within the blastoderm margin, increasing cell cohesion and thereby counteracting the effect of mitotic rounding on contact disassembly. Overall, our results identify a fluidity transition mediated by loss of cell cohesion as a critical regulator of embryo morphogenesis.
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