报告题目：Geometry-driven asymmetric cell divisions pattern cell cycles in the cleavage-stage zebrafish embryo
报告人：Carl-Philipp Heisenberg  院士 
主持人：冯新华  教授
时   间：2024年11月19日（周二）下午4点
地   点：校友楼紫金港厅
报告人简介：

Carl-Philipp Heisenberg (born 1968) is a developmental biologist who studied biology at the Ludwig-Maximilians-University in Munich and completed his doctorate in the group of Nobel laureate Christiane Nüsslein-Volhard at the Max-Planck-Institute for developmental biology in Tübingen in 1997. In 2001, he became research group leader and Emmy Noether Junior Professor at the Max-Planck-Institute for Molecular Cell Biology and Genetics in Dresden. In 2010, he started as a Professor at the Institute of Science and Technology (IST) Austria in Klosterneuburg. Heisenberg received an ERC Advanced Grant in 2017 from the European Research Council and, in the same year, the “Würdigungspreis” from Lower Austria. Since 2015 he has been a member of the German Academy of Sciences Leopoldina. In 2018, he joined the Board of Reviewing Editors of the journal Science and, in 2019, received the Carus Medal from the Leopoldina.

Abstract:

In many organisms, the initial embryonic cell cycles are highly synchronized but gradually metasynchronize. Embryos with perturbed synchrony fail development, suggesting that this is a phenomenon of fundamental importance. Yet, the mechanisms synchronizing cell cycles and the detailed developmental role thereof are poorly understood. In zebrafish, as cell cycles metasynchronize, they produce radial mitotic waves originating at the animal pole (AP). We show that these waves are produced largely, if not exclusively, cell-autonomously due to disproportionately greater S-phase lengthening away from AP. In fact, introducing cell coupling reshapes the wave and, surprisingly, re-positions its origin to the margin. Furthermore, the gradient of S-phase lengths arises due to a reciprocal cell volume gradient produced by asymmetric cell divisions in the early embryo guided by its geometry. Finally, we report that this volume gradient likely patterns zygotic transcription onset in the embryo, such that the smaller, marginal cells commence zygotic transcription first. This potentially introduces a new axis of fate specification, where an accumulation of zygotically expressed fate determinants, such as Nodal, away from AP could propel the marginal cells and the yolk syncytial layer (YSL) toward adopting/promoting a mesendodermal fate. Thus, our study provides insights into how the geometry of the early embryo could be interpreted to generate the embryonic fate map, laying down the blueprint for animal development.