Adherens Junction Length during Tissue Contraction Is Controlled by the Mechanosensitive Activity of Actomyosin and Junctional Recycling

被引:51
作者
Sumi, Angughali [1 ]
Hayes, Peran [1 ]
D'Angelo, Arturo [1 ]
Colombelli, Julien [3 ]
Salbreux, Guillaume [4 ]
Dierkes, Kai [1 ]
Solon, Jerome [1 ,2 ]
机构
[1] Barcelona Inst Sci & Technol, Ctr Genom Regulat CRG, Dr Aiguader 88, Barcelona 08003, Spain
[2] UPF, Barcelona 08003, Spain
[3] Barcelona Inst Sci & Technol, Inst Res Biomed IRB Barcelona, Barcelona 08028, Spain
[4] Francis Crick Inst, 1 Midland Rd, London NW1 1AT, England
基金
英国惠康基金;
关键词
DORSAL CLOSURE; APICAL CONSTRICTION; CELL; MORPHOGENESIS; DROSOPHILA; FORCES; MYOSIN; ADHESION; TRANSMISSION; ENDOCYTOSIS;
D O I
10.1016/j.devcel.2018.10.025
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
During epithelial contraction, cells generate forces to constrict their surface and, concurrently, fine-tune the length of their adherens junctions to ensure force transmission. While many studies have focused on understanding force generation, little is known on how junctional length is controlled. Here, we show that, during amnioserosa contraction in Drosophila dorsal closure, adherens junctions reduce their length in coordination with the shrinkage of apical cell area, maintaining a nearly constant junctional straightness. We reveal that junctional straightness and integrity depend on the endocytic machinery and on the mechanosensitive activity of the actomyosin cytoskeleton. On one hand, upon junctional stretch and decrease in E-cadherin density, actomyosin relocalizes from the medial area to the junctions, thus maintaining junctional integrity. On the other hand, when junctions have excess material and ruffles, junction removal is enhanced, and high junctional straightness and tension are restored. These two mechanisms control junctional length and integrity during morphogenesis.
引用
收藏
页码:453 / +
页数:14
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