In a first blog post (1), you mocked and ridiculed our scientific work. Apparently you had not even read the article (2). Now that you have read the article, you seem to find some merit to this work (3), and realize that it is based on experimental work on actual embryos, and not experiments on rubber as you seem to have thought. The rubber examples come only by the end of the article, in the conclusion section, to illustrate the phenomenon.
You challenge us to explain : “(1) how these changes in body plans could become encoded in the DNA, (2) why [our] theory is not Lamarckian.”

To be honnest, these questions by the end of your last blog post are as stupid as is arrogant and absurd the sentence : “After a review of the paper, published in European Physical Journal E, we can report that our original coverage was entirely correct. »

Nowhere in our article is darwinism questionned, and nowhere in our article is lamarckism put forward. I do not even understand what you mean by lamarckism in this instance. We are adressing the movements in a blastula, at an early developmental stage. Movements at the blastula stage do not occur by free will of the blastula, nor is anyone pulling on the ectoderm “from the outside”. Movements in the blastula at any generation occur by the live activity of the blastula at that generation, as defined by the molecular content at that moment, in particular the genetic content. All the examples and challenges which you suggest (such as your volvox example) are completely nonsensical.

Now, this being said, at early developmental and evolutionary stage, we assume that masses of living cells were simpler. In effect, vertebrate blastulas are round.


It is unlikely that this roundness is controlled by genes. We show that at early developmental stages, cells are organized in rings, much like tree rings. This makes sense, and it is also unlikely that genes control specifically the ring symmetry of the cells. In addition, the cell size varies from the inside towards the periphery. Cells are smaller internally and larger externally.



It is also unlikely that such a trend is genetically controlled. It is just an effect of cell crowding. Now, we also show that cells size vary stepwise, in a regular manner, with cells having roughly the sizes 5-10-15-20 microns in the rings, which has the flavour of a physical variation due to imprint of the early divisions in the entire blastula (if these dimensions were under genetic control, one would hardly understand why the variation is regular). We assume however that there exists an antero-posterior asymmetry, which is indeed of genetic origin, and related to the second cleavage, which is asymmetrical.

In a previous article (4), and in this one, we show that morphogenesis occurs by a Marangoni effect between the observed rings (gradient of surface tension) which triggers a vortex movement (emergent flow) which is nowhere coded as such.

Measurement and modelling of the vortex movements in early blastulas © VF/CNRS/MSC/BIOSYSTEMS Measurement and modelling of the vortex movements in early blastulas © VF/CNRS/MSC/BIOSYSTEMS


Stated otherwise, there is some sort of a “code” if you insist, in the presence of rings, but the algorithm to decipher the code is entirely physical and starts by a hydrodynamic flow (the vectors of the field are not “controlled” locally). This flow continues by a spontaneous spread of mesoderm, and the spread of mesoderm pulls and folds the embryo along the prepatterned boundaries of elastic contrast, locked at boundaries between rings.

It suffices to increase the magnitude of the driving force (mesodermal pull) to generate such animals as cephalochordates, once the buckling threshold is crossed. This work assumes that cell motility increased somehow such that the driving force for morphogenesis reached the buckling level. Of course, this force is genetically coded. Which should please you considerably.
However, if you like scientific reasoning, you might be aware of recent work suggesting that the cambrian explosion occured as a consequence of raising levels of oxygen in the atmosphere, which favored a metabolism based on respiration, as opposed as a metabolism based on fermentation, which is much less efficient. In this view, animal morphogenesis may have occurred without specific genetic mutations : everything might have been ready for millions of years when the cell strength became epigenetically large enough to start the Marangoni movements of the rings, which lead eventually to the buckling of the blastula. But I agree this is a speculation, as is any form of reasoning about what happenned 600 millions years ago (5).
Vincent Fleury


2.Buckling along boundaries of elastic contrast as a mechanism for early vertebrate morphogenesis, Vincent Fleury, Nicolas R. Chevalier, Fabien Furfaro et Jean-Loup Duband. European Physical Journal E, 38, 6, on line 12 february 2015.


4.Clarifying tetrapod embryogenesis by a dorso-ventral analysis of the tissue flows during early stages of chicken development, Biosystems, V. Fleury, Special issue “Morphogenesis”, 109, (3), 460-474 (2012).

5. A second reply to the continuing nonsense of these guys can be found here :


Le Club est l'espace de libre expression des abonnés de Mediapart. Ses contenus n'engagent pas la rédaction.

Les commentaires sont réservés aux abonnés.