@article{5789,
  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.},
  author       = {Petridou, Nicoletta and Grigolon, Silvia and Salbreux, Guillaume and Hannezo, Edouard B and Heisenberg, Carl-Philipp J},
  issn         = {14657392},
  journal      = {Nature Cell Biology},
  pages        = {169–178},
  publisher    = {Nature Publishing Group},
  title        = {{Fluidization-mediated tissue spreading by mitotic cell rounding and non-canonical Wnt signalling}},
  doi          = {10.1038/s41556-018-0247-4},
  volume       = {21},
  year         = {2019},
}

@article{678,
  abstract     = {The seminal observation that mechanical signals can elicit changes in biochemical signalling within cells, a process commonly termed mechanosensation and mechanotransduction, has revolutionized our understanding of the role of cell mechanics in various fundamental biological processes, such as cell motility, adhesion, proliferation and differentiation. In this Review, we will discuss how the interplay and feedback between mechanical and biochemical signals control tissue morphogenesis and cell fate specification in embryonic development.},
  author       = {Petridou, Nicoletta and Spiro, Zoltan P and Heisenberg, Carl-Philipp J},
  issn         = {14657392},
  journal      = {Nature Cell Biology},
  number       = {6},
  pages        = {581 -- 588},
  publisher    = {Nature Publishing Group},
  title        = {{Multiscale force sensing in development}},
  doi          = {10.1038/ncb3524},
  volume       = {19},
  year         = {2017},
}

@article{661,
  abstract     = {During embryonic development, mechanical forces are essential for cellular rearrangements driving tissue morphogenesis. Here, we show that in the early zebrafish embryo, friction forces are generated at the interface between anterior axial mesoderm (prechordal plate, ppl) progenitors migrating towards the animal pole and neurectoderm progenitors moving in the opposite direction towards the vegetal pole of the embryo. These friction forces lead to global rearrangement of cells within the neurectoderm and determine the position of the neural anlage. Using a combination of experiments and simulations, we show that this process depends on hydrodynamic coupling between neurectoderm and ppl as a result of E-cadherin-mediated adhesion between those tissues. Our data thus establish the emergence of friction forces at the interface between moving tissues as a critical force-generating process shaping the embryo.},
  author       = {Smutny, Michael and Ákos, Zsuzsa and Grigolon, Silvia and Shamipour, Shayan and Ruprecht, Verena and Capek, Daniel and Behrndt, Martin and Papusheva, Ekaterina and Tada, Masazumi and Hof, Björn and Vicsek, Tamás and Salbreux, Guillaume and Heisenberg, Carl-Philipp J},
  issn         = {14657392},
  journal      = {Nature Cell Biology},
  pages        = {306 -- 317},
  publisher    = {Nature Publishing Group},
  title        = {{Friction forces position the neural anlage}},
  doi          = {10.1038/ncb3492},
  volume       = {19},
  year         = {2017},
}