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Bensimon, D.

Publications and source records attributed to Bensimon, D..

2 recordsLinked to original sources

Quantitative study of the somitogenetic wavefront in zebrafish

A quantitative description of the molecular networks that sustain morphogenesis is one of the challenges of developmental biology. Specifically, a molecular understanding of the segmentation of the antero-posterior axis in vertebrates has yet to be achieved. This process known as somitogenesis is believed to result from the interactions between a genetic oscillator and a posterior-moving determination wavefront. Here we quantitatively study and perturb the network in zebrafish that sustains this wavefront and compare our observations to a model whereby the wavefront is due to a switch between stable states resulting from reciprocal negative feedbacks of Retinoic Acid (RA) on the activation of ERK and of ERK on RA synthesis. This model quantitatively accounts for the near linear shortening of the post-somitic mesoderm (PSM) in response to the observed exponential decrease during somitogenesis of the mRNA concentration of a morphogen (Fgf8). It also accounts for the observed dynamics of the PSM when the molecular components of the network are perturbed. The generality of our model and its robustness allows for its test in other model organisms.

developmental biology

Asymmetric adhesion of rod-shaped bacteria controls microcolony morphogenesis

Bacterial biofilms are spatially structured communities, within which bacteria can differentiate depending on environmental conditions. During biofilm formation, bacteria attach to a surface and use cell-cell contacts to convey the signals required for the coordination of biofilm morphogenesis. How bacteria can maintain both substrate adhesions and cell-cell contacts during the expansion of a microcolony is still a critical yet poorly understood phenomenon. Here, we describe the development of time-resolved methods to measure substrate adhesion at the single cell level during the formation of E. coli and P. aeruginosa microcolonies. We show that bacterial adhesion is asymmetrically distributed along the cell body. Higher adhesion forces at old poles put the daughter cells under tension and force them to slide along each other. These rearrangements increase cell-cell contacts and the circularity of the colony. We propose a mechanical model based on the microscopic details of adhesive links, which recapitulates microcolony morphogenesis and quantitatively predicts bacterial adhesion from simple time lapse movies. These results explain how the distribution of adhesion forces at the subcellular level directs the shape of bacterial colonies, which ultimately dictates the circulation of secreted signals.

biophysics