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Nat Commun. 2018 Sep 10;9(1):3295. doi: 10.1038/s41467-018-05605-7.

AIP1 and cofilin ensure a resistance to tissue tension and promote directional cell rearrangement.

Author information

1
Institute for Integrated Cell-Material Sciences (WPI-iCeMS), Kyoto University, Kyoto, 606-8501, Japan.
2
Institute for Integrated Cell-Material Sciences (WPI-iCeMS), Kyoto University, Kyoto, 606-8501, Japan. ksugimura@icems.kyoto-u.ac.jp.
3
JST PRESTO, Tokyo, 102-0075, Japan. ksugimura@icems.kyoto-u.ac.jp.

Abstract

In order to understand how tissue mechanics shapes animal body, it is critical to clarify how cells respond to and resist tissue stress when undergoing morphogenetic processes, such as cell rearrangement. Here, we address the question in the Drosophila wing epithelium, where anisotropic tissue tension orients cell rearrangements. We found that anisotropic tissue tension localizes actin interacting protein 1 (AIP1), a cofactor of cofilin, on the remodeling junction via cooperative binding of cofilin to F-actin. AIP1 and cofilin promote actin turnover and locally regulate the Canoe-mediated linkage between actomyosin and the junction. This mechanism is essential for cells to resist the mechanical load imposed on the remodeling junction perpendicular to the direction of tissue stretching. Thus, the present study delineates how AIP1 and cofilin achieve an optimal balance between resistance to tissue tension and morphogenesis.

PMID:
30202062
PMCID:
PMC6131156
DOI:
10.1038/s41467-018-05605-7
[Indexed for MEDLINE]
Free PMC Article

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