RT Journal Article
SR Electronic
T1 Mechanical coupling of supracellular stress amplification and tissue fluidization during exit from quiescence
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2021.10.19.464930
DO 10.1101/2021.10.19.464930
A1 Emma Lång
A1 Christian Pedersen
A1 Anna Lång
A1 Pernille Blicher
A1 Arne Klungland
A1 Andreas Carlson
A1 Stig Ove Bøe
YR 2021
UL http://biorxiv.org/content/early/2021/11/22/2021.10.19.464930.abstract
AB Cellular quiescence is a state of reversible cell cycle arrest that is associated with tissue dormancy. Timely regulated entry into and exit from quiescence is important for processes such as tissue homeostasis, tissue repair, stem cell maintenance, developmental processes and immunity. Here we show that quiescent human keratinocyte monolayers contain an actinomyosin-based system that facilitates global viscoelastic flow upon serum-stimulated exit from quiescence. Mechanistically, serum exposure causes rapid amplification of pre-existing contractile sites leading to a burst in monolayer stress that subsequently drives monolayer fluidization. The stress magnitude after quiescence exit correlates with quiescence depth, and a critical stress level must be reached to overcome the cell sheet displacement barrier. The study shows that static quiescent cell monolayers are mechanically poised for motility and identifies global stress amplification as a mechanism for tissue fluidization.Competing Interest StatementThe authors have declared no competing interest.