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整数拓扑缺陷提供了一种量化和分类活性细胞单层的方法。

Integer topological defects offer a methodology to quantify and classify active cell monolayers.

作者信息

Zhao Zihui, Li He, Yao Yisong, Zhao Yongfeng, Serra Francesca, Kawaguchi Kyogo, Zhang Hepeng, Sano Masaki

机构信息

School of Physics and Astronomy, Shanghai Jiao Tong University, Shanghai, China.

Institute of Natural Sciences, Shanghai Jiao Tong University, Shanghai, China.

出版信息

Nat Commun. 2025 Mar 12;16(1):2452. doi: 10.1038/s41467-025-57783-w.

DOI:10.1038/s41467-025-57783-w
PMID:40069207
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11897356/
Abstract

Monolayers of confluent elongated cells are frequently considered active nematics, featuring topological defects. In extensile systems, where cells extend further along their long axis, they can accumulate at defects and escape from defects. Nevertheless, collective dynamics surrounding integer defects remain insufficiently understood. We induce diverse  + 1 topological defects (asters, spirals, and targets) within neural progenitor cell monolayers using microfabricated patterns. Remarkably, cells migrate toward the cores of all  + 1 defects, challenging existing theories and conventional extensile/contractile dichotomy, which predicts escape from highly bent spirals and targets. By combining experiments and a continuum theory derived from a cell-level model, we identify previously overlooked nonlinear active forces driving this unexpected accumulation toward defect cores, providing a unified framework to explain cell behavior across defect types. Our findings establish  + 1 defects as probes to uncover key nonlinear features of active nematics, offering a methodology to characterize and classify cell monolayers.

摘要

汇合伸长细胞的单层通常被认为是具有拓扑缺陷的活性向列相。在拉伸系统中,细胞沿其长轴进一步延伸,它们可以在缺陷处聚集并从缺陷处逃逸。然而,围绕整数缺陷的集体动力学仍未得到充分理解。我们使用微加工图案在神经祖细胞单层中诱导出各种 +1 拓扑缺陷(星状体、螺旋体和靶状体)。值得注意的是,细胞会向所有 +1 缺陷的核心迁移,这挑战了现有理论和传统的拉伸/收缩二分法,后者预测细胞会从高度弯曲的螺旋体和靶状体中逃逸。通过结合实验和从细胞水平模型推导出来的连续体理论,我们确定了以前被忽视的驱动这种意外向缺陷核心积累的非线性活性力,提供了一个统一的框架来解释跨缺陷类型的细胞行为。我们的发现将 +1 缺陷确立为揭示活性向列相关键非线性特征的探针,提供了一种表征和分类细胞单层的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/11897356/0a3faba254f9/41467_2025_57783_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/11897356/3a7f19382fea/41467_2025_57783_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/11897356/57fb9001124e/41467_2025_57783_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/11897356/6c593dbc72b3/41467_2025_57783_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/11897356/0a3faba254f9/41467_2025_57783_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/11897356/3a7f19382fea/41467_2025_57783_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/11897356/57fb9001124e/41467_2025_57783_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/11897356/6c593dbc72b3/41467_2025_57783_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/11897356/0a3faba254f9/41467_2025_57783_Fig4_HTML.jpg

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本文引用的文献

1
Integer Topological Defects Reveal Antisymmetric Forces in Active Nematics.整数拓扑缺陷揭示活性向列相中的反对称力。
Phys Rev Lett. 2024 Dec 31;133(26):268301. doi: 10.1103/PhysRevLett.133.268301.
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Local polar order controls mechanical stress and triggers layer formation in Myxococcus xanthus colonies.局部极性秩序控制机械应力并触发黄色粘球菌菌落中的层形成。
Nat Commun. 2025 Jan 22;16(1):952. doi: 10.1038/s41467-024-55806-6.
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Stress-shape misalignment in confluent cell layers.细胞层融合时的应力-形状失配。
Nat Commun. 2024 Apr 29;15(1):3628. doi: 10.1038/s41467-024-47702-w.
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Migration and division in cell monolayers on substrates with topological defects.具有拓扑缺陷基底上细胞单层的迁移和分裂。
Proc Natl Acad Sci U S A. 2023 Jul 25;120(30):e2301197120. doi: 10.1073/pnas.2301197120. Epub 2023 Jul 18.
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Collagen Fibril Orientation Instructs Fibroblast Differentiation Via Cell Contractility.胶原纤维取向通过细胞收缩性指导成纤维细胞分化。
Adv Sci (Weinh). 2023 Aug;10(22):e2301353. doi: 10.1002/advs.202301353. Epub 2023 May 30.
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Phys Rev Lett. 2022 Feb 18;128(7):078001. doi: 10.1103/PhysRevLett.128.078001.
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Integer topological defects organize stresses driving tissue morphogenesis.整数拓扑缺陷组织驱动组织形态发生的应力。
Nat Mater. 2022 May;21(5):588-597. doi: 10.1038/s41563-022-01194-5. Epub 2022 Feb 10.
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