Biology subjects

Collinet, C.

Publications and source records attributed to Collinet, C..

5 recordsLinked to original sources

bioRxiv2025

Spatial patterning of contractility by a mechanogen gradient underlies Drosophila gastrulation

During development cell deformations are spatially organized, however, how cellular mechanics is spatially controlled is unclear. Spatial control of cell identity often determines local cellular mechanics in a two-tiered mechanism (1). Theoretical studies also proposed that molecular gradients, so called "mechanogens", spatially control mechanics (2, 3). We report evidence of such a "mechanogen" required for Drosophila gastrulation. We show that the GPCR ligand Fog, expressed in the posterior endoderm (4-6), diffuses and acts in a concentration-dependent manner to activate actomyosin contractility at a distance during a wave of tissue invagination. While Fog is uniformly distributed in the extracellular space, it forms a surface-bound gradient that activates Myosin-II via receptor oligomerization. This activity gradient self-renews as the wave propagates and is shaped by both receptor endocytosis and a feedback mechanism involving adhesion to the vitelline membrane by integrins. This exemplifies how chemical, mechanical and geometrical cues underly the emergence of a self-organized mechanogen activity gradient.

developmental biology↗

bioRxiv2023

Mechanical regulation of substrate adhesion and de-adhesion drives a cell contractile wave during tissue morphogenesis

During morphogenesis tissue-scale forces drive large-scale deformations, yet how these forces arise from the local interplay between cellular contractility and adhesion is poorly understood. In the posterior endoderm of Drosophila embryos, a self-organized tissue-scale wave of actomyosin contractility and cell invagination is coupled with adhesion to the surrounding vitelline membrane to drive the polarized tissue deformation. We report here that this process emerges at the subcellular level from the mechanical coupling between Myosin-II activation and sequential adhesion/de-adhesion to the vitelline membrane. At the wavefront, integrin focal complexes anchor the actin cortex to the vitelline membrane and promote activation of Myosin-II, which in turn enhances adhesion in a positive feedback loop. Subsequently, upon detachment, cortex contraction and advective flow further amplify Myosin-II levels. Prolonged contact with the vitelline membrane increases the duration of the integrin-Myosin-II feedback, integrin adhesion and thus slows down cell detachment and wave propagation of the invagination. Finally, we show that the angle of cell detachment changes as a function of the strength of adhesion and modifies the tensile forces required for detachment to maintain wave propagation. This illustrates how the tissue-scale wave arises from subcellular mechanochemical feedbacks and tissue geometry.

developmental biology↗

bioRxiv2018

Force inference predicts local and tissue-scale stress patterns in epithelia

Morphogenesis relies on the active generation of forces, and the transmission of these forces to surrounding cells and tissues. Hence measuring forces directly in developing embryos is an essential task to study the mechanics of development. Among the experimental techniques that have emerged to measure forces in epithelial tissues, force inference is particularly appealing. Indeed it only requires a snapshot of the tissue, as it relies on the topology and geometry of cell contacts, assuming that forces are balanced at each vertex. However, establishing force inference as a reliable technique requires thorough validation in multiple conditions. Here we performed systematic comparisons of force inference with laser ablation experiments in three distinct Drosophila epithelia. We show that force inference accurately predicts single junction tensions, tension patterns in stereotyped groups of cells, and tissue-scale stress patterns, in wild type and mutant conditions. We emphasize its ability to capture the distribution of forces at different scales from a single image, which gives it a critical advantage over perturbative techniques such as laser ablation. Our results demonstrate that force inference is a reliable and efficient method to quantify the mechanics of epithelial tissues during morphogenesis.

biophysics↗

bioRxiv2018

Transcriptional initiation and mechanically driven self-propagation of a tissue contractile wave during axis elongation

Tissue morphogenesis emerges from coordinated cell shape changes driven by actomyosin contraction1, 2. Spatial patterns of gene expression regionalize and polarize cell behaviours, such as apical constriction in the ventral mesoderm and cell intercalation in the lateral ectoderm of Drosophila3. Thus, tissue dynamics is largely governed genetically. Actomyosin contractile networks drive cell and tissue-level shape changes and can respond to mechanical stimuli 4-9. However how genetic information and mechanical control drive tissue-level morphogenesis is not well understood. Here we report two phases and modalities of Rho1 and non-muscle MyosinII (MyoII) activation in the Drosophila posterior endoderm. First, Rho1/MyoII are induced apically in a spatially restricted primordium region via localized transcription of the GPCR ligand Fog. Second, a tissue-scale travelling wave of Rho1/MyoII activation and cell invagination progresses anteriorly across the dorsal epithelium at a constant speed of 1 cell every 3 minutes. Remarkably, the MyoII wave does not require sustained gene transcription, and is also insensitive to perturbations in the level and pattern of Fog expression. Thus, while fog transcription initiates Rho1/MyoII activation in the primordium, Fog delivery does not govern wave dynamics. Instead, perturbing the mechanical environment of the endoderm impaired MyoII wave dynamics. MyoII inhibition blocked acute Rho1 activation and propagation, suggesting that MyoII contractility provides both local feedback amplification and spatial coupling necessary for wave progression. Finally, we identify a cycle of 3D cell deformations that link MyoII activation and invagination in one row of cells to vitelline membrane attachment, apical spreading, MyoII activation and invagination in the next row, to drive anterior progression of the invagination wave. Thus endoderm morphogenesis emerges from local transcriptional initiation and a mechanically driven travelling cycle of cell contraction and deformation.

developmental biology↗

bioRxiv2017

Viscoelastic dissipation stabilizes cell shape changes during tissue morphogenesis

Tissue morphogenesis relies on the production of active cellular forces. Understanding how such forces are mechanically converted into cell shape changes is essential to our understanding of morphogenesis. Here we use Myosin II pulsatile activity during Drosophila embryogenesis to study how transient forces generate irreversible cell shape changes. Analyzing the dynamics of junction shortening and elongation resulting from Myosin II pulses, we find that long pulses yield less reversible deformations, typically a signature of dissipative mechanics. This is consistent with a simple viscoelastic description, which we use to model individual shortening and elongation events. The model predicts that dissipation typically occurs on the minute timescale, a timescale commensurate with that of force generation by Myosin II pulses. We test this estimate by applying time-controlled forces on junctions with optical tweezers. Our results argue that active junctional deformation is stabilized by dissipation. Hence, tissue morphogenesis requires coordination between force generation and dissipation.

developmental biology↗