Detail of fig6a_upper
Project
Title
Time-lapse images of Lifeact-EGFP expressed in HT29 cells during nocodazole treatment in αE-catenin depleted cells
Description
NA
Release, Updated
2018-11-14
License
CC BY
Kind
Image data
based on Experiment
File Formats
Data size
45.9 MB
Datatype
cell dynamics
Molecular Function (MF)
Biological Process (BP)
-
Cellular Component (CC)
apical junction complex
(
GO:0043296
)
Biological Imaging Method
XYZ Scale
XY: 353 micrometer/pixel, Z: NA micrometer/slice
T scale
120 second for each time interval
Image Acquisition
Experiment type
TimeLapse
Microscope type
ConfocalMicroscope
Acquisition mode
LaserScanningConfocalMicroscopy
Contrast method
DIC
Microscope model
Olympus LCV100 or Olympus IX81 + Yokogawa CSU-W1
Detector model
Olympus DP30 or ImagEM-IK
Objective model
Olympus UAPOx40/340 or PLANAPO N x60/1.42 oil lens
Filter set
Summary of Methods
See details in Ito et al. (2017) Nat Commun, 8(1): 1834-1849.
Related paper(s)
Shoko Ito, Satoru Okuda, Masako Abe, Mari Fujimoto, Tetsuo Onuki, Tamako Nishimura, Masatoshi Takeichi (2017) Induced cortical tension restores functional junctions in adhesion-defective carcinoma cells., Nature communications, Volume 8, Number 1, pp. 1834
Published in 2017 Nov 28 (Electronic publication in Nov. 28, 2017, midnight )
- doi: 10.1038/s41467-017-01945-y
-
pmid: 29184140
(Abstract) Normal epithelial cells are stably connected to each other via the apical junctional complex (AJC). AJCs, however, tend to be disrupted during tumor progression, and this process is implicated in cancer dissemination. Here, using colon carcinoma cells that fail to form AJCs, we investigated molecular defects behind this failure through a search for chemical compounds that could restore AJCs, and found that microtubule-polymerization inhibitors (MTIs) were effective. MTIs activated GEF-H1/RhoA signaling, causing actomyosin contraction at the apical cortex. This contraction transmitted force to the cadherin-catenin complex, resulting in a mechanosensitive recruitment of vinculin to cell junctions. This process, in turn, recruited PDZ-RhoGEF to the junctions, leading to the RhoA/ROCK/LIM kinase/cofilin-dependent stabilization of the junctions. RhoGAP depletion mimicked these MTI-mediated processes. Cells that normally organize AJCs did not show such MTI/RhoA sensitivity. Thus, advanced carcinoma cells require elevated RhoA activity for establishing robust junctions, which triggers tension-sensitive reorganization of actin/adhesion regulators.(MeSH Terms)
- Actin Cytoskeleton/metabolism
- Actin Cytoskeleton/ultrastructure
- Actin Depolymerizing Factors/metabolism
- Actins/metabolism
- Actomyosin/metabolism
- Adherens Junctions/metabolism[major]
- Adherens Junctions/ultrastructure
- Biomechanical Phenomena
- Caco-2 Cells
- Cadherins/metabolism
- Cell Adhesion/physiology[major]
- Cell Adhesion Molecules/metabolism[major]
- Cell Line, Tumor
- Colonic Neoplasms/metabolism[major]
- Colonic Neoplasms/pathology
- Cytoskeletal Proteins/metabolism[major]
- Epithelial Cells/metabolism
- Guanine Nucleotide Exchange Factors/metabolism
- HT29 Cells/cytology
- HT29 Cells/drug effects
- HT29 Cells/physiology[major]
- Humans
- Intercellular Junctions/physiology[major]
- Lim Kinases/metabolism
- Microtubules
- Myosin Type II/metabolism
- Nocodazole/pharmacology
- Signal Transduction
- Vinculin/metabolism
- rho-Associated Kinases/metabolism
- rhoA GTP-Binding Protein/metabolism
Contact
Masatoshi Takeichi
, RIKEN
, Center for Biosystems Dynamics Research
, Laboratory for Cell Adhesion and Tissue Patterning
Contributors
Shoko Ito, Satoru Okuda, Masako Abe, Mari Fujimoto, Tetsuo Onuki, Tamako Nishimura, Masatoshi Takeichi
OMERO Dataset
OMERO Project
Source