Mécanique du développement des mammifères

Publications de l’équipe

Année de publication : 2013

Jean-Léon Maître, Hélène Berthoumieux, Simon Frederick Gabriel Krens, Guillaume Salbreux, Frank Jülicher, Ewa Paluch, Carl-Phillip Heisenberg (2013 Mar 5)

[Cell adhesion mechanics of zebrafish gastrulation].

Médecine sciences : M/S : 147-50 : DOI : 10.1051/medsci/2013292011 En savoir plus


Année de publication : 2012

Jean-Léon Maître, Hélène Berthoumieux, Simon Frederik Gabriel Krens, Guillaume Salbreux, Frank Jülicher, Ewa Paluch, Carl-Philipp Heisenberg (2012 Aug 28)

Adhesion functions in cell sorting by mechanically coupling the cortices of adhering cells.

Science (New York, N.Y.) : 253-6 : DOI : 10.1126/science.1225399 En savoir plus

Differential cell adhesion and cortex tension are thought to drive cell sorting by controlling cell-cell contact formation. Here, we show that cell adhesion and cortex tension have different mechanical functions in controlling progenitor cell-cell contact formation and sorting during zebrafish gastrulation. Cortex tension controls cell-cell contact expansion by modulating interfacial tension at the contact. By contrast, adhesion has little direct function in contact expansion, but instead is needed to mechanically couple the cortices of adhering cells at their contacts, allowing cortex tension to control contact expansion. The coupling function of adhesion is mediated by E-cadherin and limited by the mechanical anchoring of E-cadherin to the cortex. Thus, cell adhesion provides the mechanical scaffold for cell cortex tension to drive cell sorting during gastrulation.


Année de publication : 2011

Petra Stockinger, Jean-Léon Maître, Carl-Philipp Heisenberg (2011 Oct 4)

Defective neuroepithelial cell cohesion affects tangential branchiomotor neuron migration in the zebrafish neural tube.

Development (Cambridge, England) : 4673-83 : DOI : 10.1242/dev.071233 En savoir plus

Facial branchiomotor neurons (FBMNs) in zebrafish and mouse embryonic hindbrain undergo a characteristic tangential migration from rhombomere (r) 4, where they are born, to r6/7. Cohesion among neuroepithelial cells (NCs) has been suggested to function in FBMN migration by inhibiting FBMNs positioned in the basal neuroepithelium such that they move apically between NCs towards the midline of the neuroepithelium instead of tangentially along the basal side of the neuroepithelium towards r6/7. However, direct experimental evaluation of this hypothesis is still lacking. Here, we have used a combination of biophysical cell adhesion measurements and high-resolution time-lapse microscopy to determine the role of NC cohesion in FBMN migration. We show that reducing NC cohesion by interfering with Cadherin 2 (Cdh2) activity results in FBMNs positioned at the basal side of the neuroepithelium moving apically towards the neural tube midline instead of tangentially towards r6/7. In embryos with strongly reduced NC cohesion, ectopic apical FBMN movement frequently results in fusion of the bilateral FBMN clusters over the apical midline of the neural tube. By contrast, reducing cohesion among FBMNs by interfering with Contactin 2 (Cntn2) expression in these cells has little effect on apical FBMN movement, but reduces the fusion of the bilateral FBMN clusters in embryos with strongly diminished NC cohesion. These data provide direct experimental evidence that NC cohesion functions in tangential FBMN migration by restricting their apical movement.

Jean-Léon Maître, Carl-Philipp Heisenberg (2011 Aug 3)

The role of adhesion energy in controlling cell-cell contacts.

Current opinion in cell biology : 508-14 : DOI : 10.1016/j.ceb.2011.07.004 En savoir plus

Recent advances in microscopy techniques and biophysical measurements have provided novel insight into the molecular, cellular and biophysical basis of cell adhesion. However, comparably little is known about a core element of cell-cell adhesion–the energy of adhesion at the cell-cell contact. In this review, we discuss approaches to understand the nature and regulation of adhesion energy, and propose strategies to determine adhesion energy between cells in vitro and in vivo.

Richard H Row, Jean-Léon Maître, Benjamin L Martin, Petra Stockinger, Carl-Philipp Heisenberg, David Kimelman (2011 Apr 6)

Completion of the epithelial to mesenchymal transition in zebrafish mesoderm requires Spadetail.

Developmental biology : 102-10 : DOI : 10.1016/j.ydbio.2011.03.025 En savoir plus

The process of gastrulation is highly conserved across vertebrates on both the genetic and morphological levels, despite great variety in embryonic shape and speed of development. This mechanism spatially separates the germ layers and establishes the organizational foundation for future development. Mesodermal identity is specified in a superficial layer of cells, the epiblast, where cells maintain an epithelioid morphology. These cells involute to join the deeper hypoblast layer where they adopt a migratory, mesenchymal morphology. Expression of a cascade of related transcription factors orchestrates the parallel genetic transition from primitive to mature mesoderm. Although the early and late stages of this process are increasingly well understood, the transition between them has remained largely mysterious. We present here the first high resolution in vivo observations of the blebby transitional morphology of involuting mesodermal cells in a vertebrate embryo. We further demonstrate that the zebrafish spadetail mutation creates a reversible block in the maturation program, stalling cells in the transition state. This mutation creates an ideal system for dissecting the specific properties of cells undergoing the morphological transition of maturing mesoderm, as we demonstrate with a direct measurement of cell-cell adhesion.


Année de publication : 2009

Elena Kardash, Michal Reichman-Fried, Jean-Léon Maître, Bijan Boldajipour, Ekaterina Papusheva, Esther-Maria Messerschmidt, Carl-Philipp Heisenberg, Erez Raz (2009 Dec 17)

A role for Rho GTPases and cell-cell adhesion in single-cell motility in vivo.

Nature cell biology : 47-53; sup pp 1-11 : DOI : 10.1038/ncb2003 En savoir plus

Cell migration is central to embryonic development, homeostasis and disease, processes in which cells move as part of a group or individually. Whereas the mechanisms controlling single-cell migration in vitro are relatively well understood, less is known about the mechanisms promoting the motility of individual cells in vivo. In particular, it is not clear how cells that form blebs in their migration use those protrusions to bring about movement in the context of the three-dimensional cellular environment. Here we show that the motility of chemokine-guided germ cells within the zebrafish embryo requires the function of the small Rho GTPases Rac1 and RhoA, as well as E-cadherin-mediated cell-cell adhesion. Using fluorescence resonance energy transfer we demonstrate that Rac1 and RhoA are activated in the cell front. At this location, Rac1 is responsible for the formation of actin-rich structures, and RhoA promotes retrograde actin flow. We propose that these actin-rich structures undergoing retrograde flow are essential for the generation of E-cadherin-mediated traction forces between the germ cells and the surrounding tissue and are therefore crucial for cell motility in vivo.


Année de publication : 2008

Clotilde Billottet, Patricia Rottiers, Florence Tatin, Christine Varon, Edith Reuzeau, Jean-Léon Maître, Frédéric Saltel, Violaine Moreau, Elisabeth Génot (2008 Apr 10)

Regulatory signals for endothelial podosome formation.

European journal of cell biology : 543-54 : DOI : 10.1016/j.ejcb.2008.02.006 En savoir plus

Podosomes are punctate actin-rich adhesion structures which spontaneously form in cells of the myelomonocytic lineage. Their formation is dependent on Src and RhoGTPases. Recently, podosomes have also been described in vascular cells. These podosomes differ from the former by the fact that they are inducible. In endothelial cells, such a signal can be provided by either constitutively active Cdc42, the PKC activator PMA or TGFbeta, depending on the model. Consequently, other regulatory pathways have been reported to contribute to podosome formation. To get more insight into the mechanisms by which podosomes form in endothelial cells, we have explored the respective contribution of signal transducers such as Cdc42-related GTPases, Smads and PKCs in three endothelial cell models. Results presented demonstrate that, in addition to Cdc42, TC10 and TCL GTPases can also promote podosome formation in endothelial cells. We also show that PKCalpha can be either necessary or entirely dispensable, depending on the cell model. In contrast, PKCdelta is essential for podosome formation in endothelial cells but not smooth muscle cells. Finally, although podosomes vary very little in their molecular composition, the signalling pathways involved in their assembly appear very diverse.