Myosin II Controls Junction Fluctuations to Guide Epithelial Tissue Ordering

被引:106
作者
Curran, Scott [1 ]
Strandkvist, Charlotte [1 ]
Bathmann, Jasper [2 ]
de Gennes, Marc [2 ]
Kabla, Alexandre [3 ]
Salbreux, Guillaume [2 ,4 ]
Baum, Buzz [1 ,4 ]
机构
[1] UCL, MRC, Lab Mol Cell Biol, Gower St, London WC1E 6BT, England
[2] Francis Crick Inst, 1 Midland Rd, London NW1 1AT, England
[3] Univ Cambridge, Dept Engn, Cambridge CB2 OQH, England
[4] UCL, Inst Phys Living Syst, Gower St, London WC1E 6BT, England
基金
英国惠康基金; 英国工程与自然科学研究理事会; 英国医学研究理事会; 英国生物技术与生命科学研究理事会;
关键词
TARGETED GENE-EXPRESSION; PLANAR CELL POLARITY; ADHERENS JUNCTIONS; MORPHOGENESIS; MECHANICS; DYNAMICS; PATTERNS; FORCES; PROLIFERATION; GROWTH;
D O I
10.1016/j.devcel.2017.09.018
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Under conditions of homeostasis, dynamic changes in the length of individual adherens junctions (AJs) provide epithelia with the fluidity required to maintain tissue integrity in the face of intrinsic and extrinsic forces. While the contribution of AJ remodeling to developmental morphogenesis has been intensively studied, less is known about AJ dynamics in other circumstances. Here, we study AJ dynamics in an epithelium that undergoes a gradual increase in packing order, without concomitant large-scale changes in tissue size or shape. We find that neighbor exchange events are driven by stochastic fluctuations in junction length, regulated in part by junctional actomyosin. In this context, the developmental increase of isotropic junctional actomyosin reduces the rate of neighbor exchange, contributing to tissue order. We propose a model in which the local variance in tension between junctions determines whether actomyosin-based forces will inhibit or drive the topological transitions that either refine or deform a tissue.
引用
收藏
页码:480 / +
页数:19
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