Polarization of Myosin II refines tissue material properties to buffer mechanical stress.

Maria Duda, Nargess Khalilgharibi, Nicolas Carpi, Anna Bove, Matthieu Piel, Guillaume Charras, Buzz Baum, Yanlan Mao

Preprint posted on December 31, 2017

How does a developing tissue protects against mechanical perturbations? Duda et al. preprint shown that Myosin II forms asymmetric cables upon tissue stretch. Surprisingly,this response depends on actin remodelling and not on main MyosinII regulators

Selected by Yara E. Sánchez Corrales


It has been very challenging to study the effects of mechanics in developmental processes because it is difficult to measure forces directly in living tissues and it is unclear whether tissue responses are a cause or a consequence of increased tension. Duda et al. preprint developed a novel approach to study tension-induced properties in a developing tissue. Using a stretching device, they were able to apply specific amounts of tension to a Drosophila wing imaginal disc and assess properties of the tissue subjected to these mechanical stimuli over short and long time scales.

Key findings

They found that Myosin II distributed asymmetrically, forming cable-like structures, parallel to the axis of the stretch (Figure 1). Over short time scales (~20 min), Myosin II polarity was proportional to the amount of stress and strain and followed cell shape. After a prolonged stretch (~3 hours), they observed a gradual decrease in Myosin II asymmetry while cell deformation was maintained. These results suggest that tension-induced Myosin II polarity followed the cell and tissue deformation over short time scales.

Figure 1. A and D) Tissue before (anchor) and after stretch (stretch); A’) Zoom from the panel A showing that Myosin II polarises upon stretch (red channel); B) Schematic of Myosin expression before (left) and after stretch (right). Panels are from the Figure 1 and 2 of the preprint; reproduced with permission. 

Why does the stretched tissue form Myosin II cables? An interesting suggestion is that this is a fast response that stiffens the tissue in order to help buffering mechanical perturbations and preserve tissue shape. When the cables were prevented to form in the whole disc pouch (by downregulating Diaphanous using RNAi), the tissue changed the aspect ratio and Myosin II depleted cells (by downregulating Myosin using zip-RNAi) became softer and more deformable.

I found very surprising that Myosin II polarisation upon stretching did not depend on main Myosin regulators (Rok, or MLCK) but required assembly/disassembly of linear actin cables generated by the formin Diaphanous.

What I like about this preprint and open questions

In my opinion, this study is important because it shows that Myosin II itself can polarise in response to mechanical stimuli in an actin dynamics dependent manner.
It would be interesting to know the localisation of Diaphanous before and after stretching. Also, I think it would be important to study the interplay of regulators and time scales over which the Myosin II/Diaphanous pathway operates in comparison to the canonical regulation.

Another important aspect of this study is that it pioneers the use of devices for applying specific levels of tension onto a developing tissue. It would be exciting to extend this approach of using novel technologies for applying specific mechanical inputs to studying the cellular and molecular basis of mechanical response during development in other tissues in Drosophila as well as other organisms.





Tags: cofilin, formin, myosin

Posted on: 18th February 2018 , updated on: 19th February 2018

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