One of the assumptions made in the paper, is that tensile stress is accumulated at the level of the extra-cellular matrix due to cells’ movements.
There is no evidence about that. To avoid any comments starting by « it is well known… », below the fold the schematic representation of filopodia driven cell movements that don’t induce permanent (and possibly cumulative) tensile stress at the substratum on witch they crawl. Schematic, that is not imaginary or by model, but, depicting experimental data from direct observations.
Maybe Fleury have another mechanism to propose, but evidence should be provided to prove that stress is accumulated to the point to impair the integrity of the basal lamina of the epiblast at the KS level. (and I’ll discuss later the partial treatment of the cellular movements). Till then, figures 5 and 6 of the paper may be considered as hypothetical.
The illustration is from Ananthakrishnan R, Ehrlicher A. The Forces Behind Cell Movement. Int J Biol Sci 2007; 3:303-317. http://www.biolsci.org/v03p0303.htm, and the legend goes:
Figure 1: A schematic of the three stages of cell movement, based on [1,12]: after determining its direction of motion, the cell extends a protusion in this direction by actin polymerization at the leading edge. It then adheres its leading edge to the surface on which it is moving and de-adheres at the cell body and rear. Finally, it pulls the whole cell body forward by contracile forces generated at the cell body and rear of the cell.
Well, polymerize, depolymerize and let the stress away.
In the same chapter I would like to add here the point of view of a moron who said once that wounds healing was a quite mechanical phenomenon, cells dropping into the hole; I’m not kidding you people. Yep, that kind of morons exists nowadays, not yet extinct. There is a quite interesting website from Gabriel Fenteany’s team at the University of Connecticut to visit about this subject.
And this isn’t a quite different matter when it helps to reveal scientific illiteracy 😉