@article{9006,
  abstract     = {Cytoplasm is a gel-like crowded environment composed of various macromolecules, organelles, cytoskeletal networks, and cytosol. The structure of the cytoplasm is highly organized and heterogeneous due to the crowding of its constituents and their effective compartmentalization. In such an environment, the diffusive dynamics of the molecules are restricted, an effect that is further amplified by clustering and anchoring of molecules. Despite the crowded nature of the cytoplasm at the microscopic scale, large-scale reorganization of the cytoplasm is essential for important cellular functions, such as cell division and polarization. How such mesoscale reorganization of the cytoplasm is achieved, especially for large cells such as oocytes or syncytial tissues that can span hundreds of micrometers in size, is only beginning to be understood. In this review, we will discuss recent advances in elucidating the molecular, cellular, and biophysical mechanisms by which the cytoskeleton drives cytoplasmic reorganization across different scales, structures, and species.},
  author       = {Shamipour, Shayan and Caballero Mancebo, Silvia and Heisenberg, Carl-Philipp J},
  issn         = {18781551},
  journal      = {Developmental Cell},
  number       = {2},
  pages        = {P213--226},
  publisher    = {Elsevier},
  title        = {{Cytoplasm's got moves}},
  doi          = {10.1016/j.devcel.2020.12.002},
  volume       = {56},
  year         = {2021},
}

@article{9294,
  abstract     = {In this issue of Developmental Cell, Doyle and colleagues identify periodic anterior contraction as a characteristic feature of fibroblasts and mesenchymal cancer cells embedded in 3D collagen gels. This contractile mechanism generates a matrix prestrain required for crawling in fibrous 3D environments.},
  author       = {Gärtner, Florian R and Sixt, Michael K},
  issn         = {18781551},
  journal      = {Developmental Cell},
  number       = {6},
  pages        = {723--725},
  publisher    = {Elsevier},
  title        = {{Engaging the front wheels to drive through fibrous terrain}},
  doi          = {10.1016/j.devcel.2021.03.002},
  volume       = {56},
  year         = {2021},
}

@article{8672,
  abstract     = {Cell fate transitions are key to development and homeostasis. It is thus essential to understand the cellular mechanisms controlling fate transitions. Cell division has been implicated in fate decisions in many stem cell types, including neuronal and epithelial progenitors. In other stem cells, such as embryonic stem (ES) cells, the role of division remains unclear. Here, we show that exit from naive pluripotency in mouse ES cells generally occurs after a division. We further show that exit timing is strongly correlated between sister cells, which remain connected by cytoplasmic bridges long after division, and that bridge abscission progressively accelerates as cells exit naive pluripotency. Finally, interfering with abscission impairs naive pluripotency exit, and artificially inducing abscission accelerates it. Altogether, our data indicate that a switch in the division machinery leading to faster abscission regulates pluripotency exit. Our study identifies abscission as a key cellular process coupling cell division to fate transitions.},
  author       = {Chaigne, Agathe and Labouesse, Céline and White, Ian J. and Agnew, Meghan and Hannezo, Edouard B and Chalut, Kevin J. and Paluch, Ewa K.},
  issn         = {18781551},
  journal      = {Developmental Cell},
  number       = {2},
  pages        = {195--208},
  publisher    = {Elsevier},
  title        = {{Abscission couples cell division to embryonic stem cell fate}},
  doi          = {10.1016/j.devcel.2020.09.001},
  volume       = {55},
  year         = {2020},
}

@article{8957,
  abstract     = {Global tissue tension anisotropy has been shown to trigger stereotypical cell division orientation by elongating mitotic cells along the main tension axis. Yet, how tissue tension elongates mitotic cells despite those cells undergoing mitotic rounding (MR) by globally upregulating cortical actomyosin tension remains unclear. We addressed this question by taking advantage of ascidian embryos, consisting of a small number of interphasic and mitotic blastomeres and displaying an invariant division pattern. We found that blastomeres undergo MR by locally relaxing cortical tension at their apex, thereby allowing extrinsic pulling forces from neighboring interphasic blastomeres to polarize their shape and thus division orientation. Consistently, interfering with extrinsic forces by reducing the contractility of interphasic blastomeres or disrupting the establishment of asynchronous mitotic domains leads to aberrant mitotic cell division orientations. Thus, apical relaxation during MR constitutes a key mechanism by which tissue tension anisotropy controls stereotypical cell division orientation.},
  author       = {Godard, Benoit G and Dumollard, Rémi and Munro, Edwin and Chenevert, Janet and Hebras, Céline and Mcdougall, Alex and Heisenberg, Carl-Philipp J},
  issn         = {18781551},
  journal      = {Developmental Cell},
  number       = {6},
  pages        = {695--706},
  publisher    = {Elsevier},
  title        = {{Apical relaxation during mitotic rounding promotes tension-oriented cell division}},
  doi          = {10.1016/j.devcel.2020.10.016},
  volume       = {55},
  year         = {2020},
}