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2018 ; 9
(10
): 8999-9009
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Tension-induced cytokinetic abscission in human fibroblasts
#MMPMID29507669
Gupta DK
; Du J
; Kamranvar SA
; Johansson S
Oncotarget
2018[Feb]; 9
(10
): 8999-9009
PMID29507669
show ga
Previous studies have shown that cytokinetic abscission at the end of mitosis is
executed by the ESCRT machinery in mammalian cells, and that the process is
dependent on adhesion-induced integrin signalling via a
FAK-PLK1-CEP55-TSG101/Alix-CHMP4B pathway. The present study identified an
alternative abscission mechanism driven by mechanical force. In the absence of
integrin signals (non-adherent conditions), cytokinesis in non-transformed human
fibroblasts proceeds to CEP55 accumulation at the midbody, but after prolonged
time (>3 hours) the major midbody components Aurora B, MKLP1 and CEP55 were no
longer detected in the area. Upon adhesion to fibronectin, such cells were able
to complete abscission without re-appearance of midbody proteins. Live-cell
imaging revealed that re-plating on stiff fibronectin matrix (64 KPa) allowed
>95% of the cells to complete abscission within 9 hours while the corresponding
number was 40% on soft fibronectin matrix (0.5 KPa). The cells re-plated on
poly-L-lysine were not able to generate tension and did not divide. Thus,
mechanical tension can cause cytokinetic abscission by stretching of the
intercellular bridge between the two daughter cells until it eventually ruptures
without the involvement of ESCRT complexes. Importantly, regression of the
cleavage furrow and formation of bi-nucleated cells did not occur in most of the
suspension-treated mitotic cells after re-plating on fibronectin. Septin, which
stabilizes the membrane associated with the midbody, was found to remain along
the ingressed membrane, suggesting that this filament system maintains the
membrane bridge although the midbody had dissolved, thereby preventing regression
and allowing tension to act on the narrow intercellular bridge.
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