We recently developed an optogenetic approach to modulate cell contractility with cellular precision and on fast (seconds) timescales during Drosophila embryogenesis.
For the purpose of this study, smooth muscle markers were defined as; α smooth muscle actin, calponin, caldesmon, and tropomyosin, since α smooth muscle actin is part of the contractile machinery of smooth muscle cells and calponin, caldesmon, and tropomyosin are proteins that modulate muscle cell contractility through their ability to bind to α smooth muscle actin [ 8- 10].
We address the impact of altered cell behavior using modulators of cell contractility and adhesion signaling.
Isotropic internal stresses in the blade are described by Equation 3. Preferred cell area a0 changes rapidly when cells divide and is modulated by the cell contractility ζ ¯ (see Appendix 2, 'Constitutive equation for the tissue stress').
The close association between cell prestress (or contractile mechanics) and stiffness (cortical mechanics) in adherent cells has been previously demonstrated in human airway smooth muscle cells 44; when cell contractility was modulated through the use of contractile agonists and antagonists, cellular traction forces scaled linearly with cell stiffness by MTC.
It induces oocyte maturation, stimulates sperm hypermotility, down-regulates GnRH secretion, modulates T cell functions, and adjusts human myometrial cell contractility [ 6, 7, 11- 135]35].
In contrast, the reduction in τ1 for all the cases indicates that τ1 is modulated by a complex interplay between focal adhesion disassembly and cell contractility.
For instance, PAK1 modulates the activity of myosin II (an actin interacting motor protein that can drive cell contractility), LIM-kinase (involved in actin polymerization through inactivation of cofilin family proteins) and filamin A (a large actin-binding protein that induces membrane ruffling) [ 3].
Indeed, cell shape and matrix rigidity modulate the subcellular localization of YAP and TAZ and cytoskeletal destabilization and inhibition of cell contractility inactivate YAP and TAZ [168].
Here, we investigate the role of focal adhesions, cell contractility, and actin dynamics in this process.
