@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},
}

@article{1249,
  abstract     = {Actin and myosin assemble into a thin layer of a highly dynamic network underneath the membrane of eukaryotic cells. This network generates the forces that drive cell- and tissue-scale morphogenetic processes. The effective material properties of this active network determine large-scale deformations and other morphogenetic events. For example, the characteristic time of stress relaxation (the Maxwell time τM) in the actomyosin sets the timescale of large-scale deformation of the cortex. Similarly, the characteristic length of stress propagation (the hydrodynamic length λ) sets the length scale of slow deformations, and a large hydrodynamic length is a prerequisite for long-ranged cortical flows. Here we introduce a method to determine physical parameters of the actomyosin cortical layer in vivo directly from laser ablation experiments. For this we investigate the cortical response to laser ablation in the one-cell-stage Caenorhabditis elegans embryo and in the gastrulating zebrafish embryo. These responses can be interpreted using a coarse-grained physical description of the cortex in terms of a two-dimensional thin film of an active viscoelastic gel. To determine the Maxwell time τM, the hydrodynamic length λ, the ratio of active stress ζΔμ, and per-area friction γ, we evaluated the response to laser ablation in two different ways: by quantifying flow and density fields as a function of space and time, and by determining the time evolution of the shape of the ablated region. Importantly, both methods provide best-fit physical parameters that are in close agreement with each other and that are similar to previous estimates in the two systems. Our method provides an accurate and robust means for measuring physical parameters of the actomyosin cortical layer. It can be useful for investigations of actomyosin mechanics at the cellular-scale, but also for providing insights into the active mechanics processes that govern tissue-scale morphogenesis.},
  author       = {Saha, Arnab and Nishikawa, Masatoshi and Behrndt, Martin and Heisenberg, Carl-Philipp J and Julicher, Frank and Grill, Stephan},
  journal      = {Biophysical Journal},
  number       = {6},
  pages        = {1421 -- 1429},
  publisher    = {Biophysical Society},
  title        = {{Determining physical properties of the cell cortex}},
  doi          = {10.1016/j.bpj.2016.02.013},
  volume       = {110},
  year         = {2016},
}

@article{2282,
  abstract     = {Epithelial spreading is a common and fundamental aspect of various developmental and disease-related processes such as epithelial closure and wound healing. A key challenge for epithelial tissues undergoing spreading is to increase their surface area without disrupting epithelial integrity. Here we show that orienting cell divisions by tension constitutes an efficient mechanism by which the enveloping cell layer (EVL) releases anisotropic tension while undergoing spreading during zebrafish epiboly. The control of EVL cell-division orientation by tension involves cell elongation and requires myosin II activity to align the mitotic spindle with the main tension axis. We also found that in the absence of tension-oriented cell divisions and in the presence of increased tissue tension, EVL cells undergo ectopic fusions, suggesting that the reduction of tension anisotropy by oriented cell divisions is required to prevent EVL cells from fusing. We conclude that cell-division orientation by tension constitutes a key mechanism for limiting tension anisotropy and thus promoting tissue spreading during EVL epiboly.},
  author       = {Campinho, Pedro and Behrndt, Martin and Ranft, Jonas and Risler, Thomas and Minc, Nicolas and Heisenberg, Carl-Philipp J},
  journal      = {Nature Cell Biology},
  pages        = {1405 -- 1414},
  publisher    = {Nature Publishing Group},
  title        = {{Tension-oriented cell divisions limit anisotropic tissue tension in epithelial spreading during zebrafish epiboly}},
  doi          = {10.1038/ncb2869},
  volume       = {15},
  year         = {2013},
}

@article{2950,
  abstract     = {Contractile actomyosin rings drive various fundamental morphogenetic processes ranging from cytokinesis to wound healing. Actomyosin rings are generally thought to function by circumferential contraction. Here, we show that the spreading of the enveloping cell layer (EVL) over the yolk cell during zebrafish gastrulation is driven by a contractile actomyosin ring. In contrast to previous suggestions, we find that this ring functions not only by circumferential contraction but also by a flow-friction mechanism. This generates a pulling force through resistance against retrograde actomyosin flow. EVL spreading proceeds normally in situations where circumferential contraction is unproductive, indicating that the flow-friction mechanism is sufficient. Thus, actomyosin rings can function in epithelial morphogenesis through a combination of cable-constriction and flow-friction mechanisms.},
  author       = {Behrndt, Martin and Salbreux, Guillaume and Campinho, Pedro and Hauschild, Robert and Oswald, Felix and Roensch, Julia and Grill, Stephan and Heisenberg, Carl-Philipp J},
  journal      = {Science},
  number       = {6104},
  pages        = {257 -- 260},
  publisher    = {American Association for the Advancement of Science},
  title        = {{Forces driving epithelial spreading in zebrafish gastrulation}},
  doi          = {10.1126/science.1224143},
  volume       = {338},
  year         = {2012},
}