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Tension heterogeneity directs form and fate to pattern the myocardial wall

机译：紧张异质性指示形式和命运，以模式墙壁

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摘要

How diverse cell fates and complex forms emerge and feed back to each other to sculpt functional organs remains unclear. In the developing heart, the myocardium transitions from a simple epithelium to an intricate tissue that consists of distinct layers: the outer compact and inner trabecular layers. Defects in this process, which is known as cardiac trabeculation, cause cardiomyopathies and embryonic lethality, yet how tissue symmetry is broken to specify trabecular cardiomyocytes is unknown. Here we show that local tension heterogeneity drives organ-scale patterning and cell-fate decisions during cardiac trabeculation in zebrafish. Proliferation-induced cellular crowding at the tissue scale triggers tension heterogeneity among cardiomyocytes of the compact layer and drives those with higher contractility to delaminate and seed the trabecular layer. Experimentally, increasing crowding within the compact layer cardiomyocytes augments delamination, whereas decreasing it abrogates delamination. Using genetic mosaics in trabeculation-deficient zebrafish models-that is, in the absence of critical upstream signals such as Nrg-Erbb2 or blood flow-we find that inducing actomyosin contractility rescues cardiomyocyte delamination and is sufficient to drive cardiomyocyte fate specification, as assessed by Notch reporter expression in compact layer cardiomyocytes. Furthermore, Notch signalling perturbs the actomyosin machinery in cardiomyocytes to restrict excessive delamination, thereby preserving the architecture of the myocardial wall. Thus, tissue-scale forces converge on local cellular mechanics to generate complex forms and modulate cell-fate choices, and these multiscale regulatory interactions ensure robust self-organized organ patterning.
机译：多样化的细胞命运和复杂形式出现并互相喂回雕刻功能器官仍然不清楚。在发育中的心脏中，心肌从一个简单的上皮过渡到包含明显层的复杂组织：外部紧凑和内小梁层。该过程中的缺陷被称为心脏分枝杆菌，导致心肌病和胚胎致死，然而，组织对称如何破坏以指定小梁心肌细胞未知。在这里，我们表明，局部张力异质性在斑马鱼中的心脏分枝杆菌期间驱动器官尺度图案化和细胞命运决策。组织尺度的增殖诱导的细胞挤在致密层的心肌细胞中的张力异质性，并将具有较高的收缩性的人转化为分层和种子的小梁层。在实验上，增加了紧凑层心肌细胞的拥挤，增强了分层，而减少了废除分层。在缺乏缺陷的斑马鱼模型中使用遗传马赛克 - 即在没有关键上游信号，如NRG-ERBB2或血液流动 - 我们发现诱导肌动素收缩性拯救心肌细胞分层，并且足以驱动心肌细胞命运规范，如评价在紧凑层心肌细胞中的Notch报告者表达。此外，Notch Signaling Perturbs在心肌细胞中掺入肌动酶机械，以限制过度分层，从而保持心肌壁的结构。因此，组织尺度力会聚在局部蜂窝力学上以产生复杂的形式并调节细胞 - 命运选择，并且这些多尺度调节相互作用确保了坚固的自组织器官图案。

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  • 来源
    《Nature》 |2020年第7836期|130-134|共5页
  • 作者

    Rashmi Priya; Srinivas Allanki; Alessandra Gentile; Shivani Mansingh; Veronica Uribe; Hans-Martin Maischein; Didier Y R Stainier;

  • 作者单位

    Department of Developmental Genetics Max Planck Institute for Heart and Lung Research|German Centre for Cardiovascular Research (DZHK) Partner Site Rhine-Main;

    Department of Developmental Genetics Max Planck Institute for Heart and Lung Research;

    Department of Developmental Genetics Max Planck Institute for Heart and Lung Research;

    Department of Developmental Genetics Max Planck Institute for Heart and Lung Research;

    Department of Developmental Genetics Max Planck Institute for Heart and Lung Research|Department of Physiology The University of Melbourne;

    Department of Developmental Genetics Max Planck Institute for Heart and Lung Research;

    Department of Developmental Genetics Max Planck Institute for Heart and Lung Research|German Centre for Cardiovascular Research (DZHK) Partner Site Rhine-Main;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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