@article{AndresDelgadoErnstGalardiCastillaetal.2019,
  author    = {Andr{\´e}s-Delgado, Laura and Ernst, Alexander and Galardi-Castilla, Mar{\´i}a and Bazaga, David and Peralta, Marina and M{\"u}nch, Juliane and Gonzalez-Rosa, Juan M. and Marques, In{\^e}s and Tessadori, Federico and de la Pompa, Jos{\´e} Luis and Vermot, Julien and Mercader, Nadia},
  title     = {Actin dynamics and the Bmp pathway drive apical extrusion of proepicardial cells},
  series = {Development : Company of Biologists},
  volume    = {146},
  journal   = {Development : Company of Biologists},
  number    = {13},
  publisher = {The Company of Biologists Ltd},
  address   = {Cambridge},
  issn      = {0950-1991},
  doi       = {10.1242/dev.174961},
  pages     = {15},
  year      = {2019},
  abstract  = {The epicardium, the outer mesothelial layer enclosing the myocardium, plays key roles in heart development and regeneration. During embryogenesis, the epicardium arises from the proepicardium (PE), a cell cluster that appears in the dorsal pericardium (DP) close to the venous pole of the heart. Little is known about how the PE emerges from the pericardial mesothelium. Using a zebrafish model and a combination of genetic tools, pharmacological agents and quantitative in vivo imaging, we reveal that a coordinated collective movement of DP cells drives PE formation. We found that Bmp signaling and the actomyosin cytoskeleton promote constriction of the DP, which enables PE cells to extrude apically. We provide evidence that cell extrusion, which has been described in the elimination of unfit cells from epithelia and the emergence of hematopoietic stem cells, is also a mechanism for PE cells to exit an organized mesothelium and fulfil their developmental fate to form a new tissue layer, the epicardium.},
  language  = {en}
}
@article{UribeRamadassDograetal.2018,
  author    = {Uribe, Veronica and Ramadass, Radhan and Dogra, Deepika and Rasouli, S. Javad and Gunawan, Felix and Nakajima, Hiroyuki and Chiba, Ayano and Reischauer, Sven and Mochizuki, Naoki and Stainier, Didier Y. R.},
  title     = {In vivo analysis of cardiomyocyte proliferation during trabeculation},
  series = {Development : Company of Biologists},
  volume    = {145},
  journal   = {Development : Company of Biologists},
  number    = {14},
  publisher = {Company biologists LTD},
  address   = {Cambridge},
  issn      = {0950-1991},
  doi       = {10.1242/dev.164194},
  pages     = {12},
  year      = {2018},
  abstract  = {Cardiomyocyte proliferation is crucial for cardiac growth, patterning and regeneration; however, few studies have investigated the behavior of dividing cardiomyocytes in vivo. Here, we use time-lapse imaging of beating hearts in combination with the FUCCI system to monitor the behavior of proliferating cardiomyocytes in developing zebrafish. Confirming in vitro observations, sarcomere disassembly, as well as changes in cell shape and volume, precede cardiomyocyte cytokinesis. Notably, cardiomyocytes in zebrafish embryos and young larvae mostly divide parallel to the myocardial wall in both the compact and trabecular layers, and cardiomyocyte proliferation is more frequent in the trabecular layer. While analyzing known regulators of cardiomyocyte proliferation, we observed that the Nrg/ErbB2 and TGF beta signaling pathways differentially affect compact and trabecular layer cardiomyocytes, indicating that distinct mechanisms drive proliferation in these two layers. In summary, our data indicate that, in zebrafish, cardiomyocyte proliferation is essential for trabecular growth, but not initiation, and set the stage to further investigate the cellular and molecular mechanisms driving cardiomyocyte proliferation in vivo.},
  language  = {en}
}