Centering and symmetry breaking in confined contracting actomyosin networks

eLife

Alex Mogilner¹  Bruce L Goode²  Angelika Manhart³  Niv Ierushalmi⁴  Maya Malik-Garbi⁴  Enas Abu Shah⁵  Kinneret Keren⁶ 

[1] Courant Institute of Mathematical Sciences and Department of Biology, New York University, New York, United States;Department of Biology, Brandeis University, Waltham, United States;Department of Mathematics, University College London, London, United Kingdom;Department of Physics, Technion- Israel Institute of Technology, Haifa, Israel;Department of Physics, Technion- Israel Institute of Technology, Haifa, Israel;Kennedy Institute of Rheumatology, University of Oxford, Oxford, United Kingdom;Department of Physics, Technion- Israel Institute of Technology, Haifa, Israel;Network Biology Research Laboratories and Russell Berrie Nanotechnology Institute, Technion – Israel Institute of Technology, Haifa, Israel;

关键词: actomyosin contraction;    artificial cell;    subcellular localization;    centering;    symmetry breaking;    Xenopus;   

DOI  :  10.7554/eLife.55368

来源: publisher

【 摘 要 】

Centering and decentering of cellular components is essential for internal organization of cells and their ability to perform basic cellular functions such as division and motility. How cells achieve proper localization of their organelles is still not well-understood, especially in large cells such as oocytes. Here, we study actin-based positioning mechanisms in artificial cells with persistently contracting actomyosin networks, generated by encapsulating cytoplasmic Xenopus egg extracts into cell-sized ‘water-in-oil’ droplets. We observe size-dependent localization of the contraction center, with a symmetric configuration in larger cells and a polar one in smaller cells. Centering is achieved via a hydrodynamic mechanism based on Darcy friction between the contracting network and the surrounding cytoplasm. During symmetry breaking, transient attachments to the cell boundary drive the contraction center to a polar location. The centering mechanism is cell-cycle dependent and weakens considerably during interphase. Our findings demonstrate a robust, yet tunable, mechanism for subcellular localization.

【 授权许可】

CC BY