@article{1067,
  abstract     = {Embryo morphogenesis relies on highly coordinated movements of different tissues. However, remarkably little is known about how tissues coordinate their movements to shape the embryo. In zebrafish embryogenesis, coordinated tissue movements first become apparent during “doming,” when the blastoderm begins to spread over the yolk sac, a process involving coordinated epithelial surface cell layer expansion and mesenchymal deep cell intercalations. Here, we find that active surface cell expansion represents the key process coordinating tissue movements during doming. By using a combination of theory and experiments, we show that epithelial surface cells not only trigger blastoderm expansion by reducing tissue surface tension, but also drive blastoderm thinning by inducing tissue contraction through radial deep cell intercalations. Thus, coordinated tissue expansion and thinning during doming relies on surface cells simultaneously controlling tissue surface tension and radial tissue contraction.},
  author       = {Morita, Hitoshi and Grigolon, Silvia and Bock, Martin and Krens, Gabriel and Salbreux, Guillaume and Heisenberg, Carl-Philipp J},
  issn         = {15345807},
  journal      = {Developmental Cell},
  number       = {4},
  pages        = {354 -- 366},
  publisher    = {Cell Press},
  title        = {{The physical basis of coordinated tissue spreading in zebrafish gastrulation}},
  doi          = {10.1016/j.devcel.2017.01.010},
  volume       = {40},
  year         = {2017},
}

@article{1817,
  abstract     = {Vertebrates have a unique 3D body shape in which correct tissue and organ shape and alignment are essential for function. For example, vision requires the lens to be centred in the eye cup which must in turn be correctly positioned in the head. Tissue morphogenesis depends on force generation, force transmission through the tissue, and response of tissues and extracellular matrix to force. Although a century ago D'Arcy Thompson postulated that terrestrial animal body shapes are conditioned by gravity, there has been no animal model directly demonstrating how the aforementioned mechano-morphogenetic processes are coordinated to generate a body shape that withstands gravity. Here we report a unique medaka fish (Oryzias latipes) mutant, hirame (hir), which is sensitive to deformation by gravity. hir embryos display a markedly flattened body caused by mutation of YAP, a nuclear executor of Hippo signalling that regulates organ size. We show that actomyosin-mediated tissue tension is reduced in hir embryos, leading to tissue flattening and tissue misalignment, both of which contribute to body flattening. By analysing YAP function in 3D spheroids of human cells, we identify the Rho GTPase activating protein ARHGAP18 as an effector of YAP in controlling tissue tension. Together, these findings reveal a previously unrecognised function of YAP in regulating tissue shape and alignment required for proper 3D body shape. Understanding this morphogenetic function of YAP could facilitate the use of embryonic stem cells to generate complex organs requiring correct alignment of multiple tissues. },
  author       = {Porazinski, Sean and Wang, Huijia and Asaoka, Yoichi and Behrndt, Martin and Miyamoto, Tatsuo and Morita, Hitoshi and Hata, Shoji and Sasaki, Takashi and Krens, Gabriel and Osada, Yumi and Asaka, Satoshi and Momoi, Akihiro and Linton, Sarah and Miesfeld, Joel and Link, Brian and Senga, Takeshi and Castillo Morales, Atahualpa and Urrutia, Araxi and Shimizu, Nobuyoshi and Nagase, Hideaki and Matsuura, Shinya and Bagby, Stefan and Kondoh, Hisato and Nishina, Hiroshi and Heisenberg, Carl-Philipp J and Furutani Seiki, Makoto},
  journal      = {Nature},
  number       = {7551},
  pages        = {217 -- 221},
  publisher    = {Nature Publishing Group},
  title        = {{YAP is essential for tissue tension to ensure vertebrate 3D body shape}},
  doi          = {10.1038/nature14215},
  volume       = {521},
  year         = {2015},
}

@article{1537,
  abstract     = {3D amoeboid cell migration is central to many developmental and disease-related processes such as cancer metastasis. Here, we identify a unique prototypic amoeboid cell migration mode in early zebrafish embryos, termed stable-bleb migration. Stable-bleb cells display an invariant polarized balloon-like shape with exceptional migration speed and persistence. Progenitor cells can be reversibly transformed into stable-bleb cells irrespective of their primary fate and motile characteristics by increasing myosin II activity through biochemical or mechanical stimuli. Using a combination of theory and experiments, we show that, in stable-bleb cells, cortical contractility fluctuations trigger a stochastic switch into amoeboid motility, and a positive feedback between cortical flows and gradients in contractility maintains stable-bleb cell polarization. We further show that rearward cortical flows drive stable-bleb cell migration in various adhesive and non-adhesive environments, unraveling a highly versatile amoeboid migration phenotype.},
  author       = {Ruprecht, Verena and Wieser, Stefan and Callan Jones, Andrew and Smutny, Michael and Morita, Hitoshi and Sako, Keisuke and Barone, Vanessa and Ritsch Marte, Monika and Sixt, Michael K and Voituriez, Raphaël and Heisenberg, Carl-Philipp J},
  journal      = {Cell},
  number       = {4},
  pages        = {673 -- 685},
  publisher    = {Cell Press},
  title        = {{Cortical contractility triggers a stochastic switch to fast amoeboid cell motility}},
  doi          = {10.1016/j.cell.2015.01.008},
  volume       = {160},
  year         = {2015},
}

@article{10815,
  abstract     = {In the last several decades, developmental biology has clarified the molecular mechanisms of embryogenesis and organogenesis. In particular, it has demonstrated that the “tool-kit genes” essential for regulating developmental processes are not only highly conserved among species, but are also used as systems at various times and places in an organism to control distinct developmental events. Therefore, mutations in many of these tool-kit genes may cause congenital diseases involving morphological abnormalities. This link between genes and abnormal morphological phenotypes underscores the importance of understanding how cells behave and contribute to morphogenesis as a result of gene function. Recent improvements in live imaging and in quantitative analyses of cellular dynamics will advance our understanding of the cellular pathogenesis of congenital diseases associated with aberrant morphologies. In these studies, it is critical to select an appropriate model organism for the particular phenomenon of interest.},
  author       = {Hashimoto, Masakazu and Morita, Hitoshi and Ueno, Naoto},
  issn         = {0914-3505},
  journal      = {Congenital Anomalies},
  keywords     = {Developmental Biology, Embryology, General Medicine, Pediatrics, Perinatology, and Child Health},
  number       = {1},
  pages        = {1--7},
  publisher    = {Wiley},
  title        = {{Molecular and cellular mechanisms of development underlying congenital diseases}},
  doi          = {10.1111/cga.12039},
  volume       = {54},
  year         = {2014},
}

@article{2841,
  abstract     = {In zebrafish early development, blastoderm cells undergo extensive radial intercalations, triggering the spreading of the blastoderm over the yolk cell and thereby initiating embryonic body axis formation. Now reporting in Developmental Cell, Song et al. (2013) demonstrate a critical function for EGF-dependent E-cadherin endocytosis in promoting blastoderm cell intercalations.},
  author       = {Morita, Hitoshi and Heisenberg, Carl-Philipp J},
  journal      = {Developmental Cell},
  number       = {6},
  pages        = {567 -- 569},
  publisher    = {Cell Press},
  title        = {{Holding on and letting go: Cadherin turnover in cell intercalation}},
  doi          = {10.1016/j.devcel.2013.03.007},
  volume       = {24},
  year         = {2013},
}