An Elasto-Plastic Model of Avian Gastrulation #2

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., 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 😉


10 Réponses

  1. Oops! This one is a hard one, why didn’t you ever told me about it already?

    This is about the basements of the model 😀

  2. Well, I expected you would figure this one by yourself.

    The question is why the referees of the paper didn’t discussed this point. You may publish a model, but at least make sure that the most important assumption is testable and how is a minimum to expect.

    But there is another question as interesting as this one 🙂

  3. if you are unable to see that this figure is exactly one of the motility models invoked in my paper, if you are unable to see that this figure implies a tangent stress exerted by the cell to overcome viscous drag and move forward (which appears in the wording « cortex under tension »)

    you have nothing to do in science

    you are the worst biologists I have ever met.

  4. If this is exactly the motility models invoked in your paper then there is no cumulated tensions to create forces sufficient to « crack » anything 😦

    Because the cortex under tension become loose just at the next step 🙂

    That’s the problem (for you), no stress accumulation. Are you sure you have something to do with reading/understanding? Or you just grab words around, just those fitting to your preconceived idea and letting every thing else as irrelevant?

    Please, do make an effort reading just this one sentence:  » 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.  »
    Spend as much time as necessary to understand it. There is one of the main problems of your model.

  5. […] results could validate the assumptions made.I will add a list at my conclusive remarks, including #1 and […]

  6. in the tutorial in which you found the KS and PS images you could have read such sentences :

    It is truly remarkable that cells can move horizontally within a relatively tight epithelium, the epiblast. The mechanics of such migration, including the degree to which it is truly “active” (rather than a consequence of mechanical propagation of a remote event like cell loss through ingression), is not yet understood. However, recent observations of living, Bodipy-ceramide chick embryos using two-photon microscopy have started to reveal that individual cells within the epithelium and translocate by “bobbing” up and down, as if each individual cell is a foot in a giant millipede


    These movements also deform Koller’s sickle, which appears to be subjected to a large amount of shear

    …….We also know virtually nothing about the mechanics of primitive streak elongation.


    you should stop, you know, I have no interest in this dispute and you are definitely destroying whatever may remain of your scientific reputation.

    It is not a big problem, if you do not master all these questions; the problem is the general tone and attitude. It is not at the proper level for so interesting and important things.

  7. Focus on the subject! I split it in small fragments so you would be able to understand.

    Here the question is: is there any evidence that yourclaims about how tensile stresses accumulates may have a relation with physical reality?

    If we don’t know, we don’t know and hypothesizing doesn’t make things real, as you seem to believe.

  8. oh sure : by Newton’s law, deformation rates relate to stress, that’s all.

    Weijer’s maps are proportional to shear stress.

    Are you that ignorant?

  9. Is it false that cell movements can create local stresses that are released as the cell moves forward? Leaving a substratum that is stress-free behind them?

    If false you should send mails around.
    If true you need evidence of what stresses are accumulated at the basal lamina level. You suppose it cracks. If there is something to crack at the KS level.

    You suppose also that the PS elongation is a BL crack also. It appears it isn’t ’till early stage 3, when the PS is already elongated. Disturbing for a crack’s propagation as described in fig 12 of EPMAG.
    And now, you know also, that the PS is pre-patterned by specific epiblastic cells. If you read the last reference I offered on the subject.

    a) maybe there is nothing to crack at the KS level
    b) PS formation is not a crack’s propagation as you predict
    c) we don’t even know if the « sandwich » structure you use as a base for your calculations exists.

    Shears certainly exist, the question is if there is anything that looks like your assumed shears.
    What Weijer’s maps?


  10. « Is it false that cell movements can create local stresses that are released as the cell moves forward? »

    This is certainly false, especially in this specific case.

    « Leaving a substratum that is stress-free behind them? »

    This is certainly false. If a cell is moving on a substratum, there is a stress field, even behind them. You have a completely wrong view of material science.

    The stress field created by a cell moving on a substratum is well known to be long ranged. An exact equation is in my paper, and there are references to experiments (wrinkles on soft foils).

    However, a cell at rest may be simply « at rest », with no stress anywhere, neither behind or below her.

    En résumé :

    if a cell has non zero V, let us say V=V0, there is a shear stress, below herself, and in the neighborhood outside, even surrounding her that decays like a dipole lng ranged). This is why one cell drags the other cells around (that is the first part of my paper)

    In the specific case of embryo growth, there is a non zero V almost everywhere in the blastula, and V is non zero over hours. During all this time, the blastula is under stress, everywhere. The max of shear force is around the saddle point.

    [snip by owner]

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