Biology subjects

Bailles, A.

Publications and source records attributed to Bailles, A..

3 recordsLinked to original sources

bioRxiv2024

Anisotropic stretch biases the self-organization of actin fibers in multicellular Hydra aggregates

During development, groups of cells generate shape by coordinating their mechanical properties through an interplay of self-organization and pre-patterning. Hydra displays a striking planar pattern of actin fibers at the organism scale, and mechanics influence the morphogenesis of biological structures during its pre-patterned regeneration. However, how mechanics participate in the formation of an ordered pattern from a totally disordered state remains unknown. To study this, we used cellular aggregates formed from dissociated Hydra cells, which initially lose all actin polarity yet regenerate a long-range actin pattern. We showed quantitatively that the actin meshwork evolves from a disordered symmetric state to an ordered state in which rotational symmetry is broken, and translation symmetry is partially broken, with the nematic and smectic order parameters increasing over days. During the first hours, the actin meshwork displayed spatial heterogeneity in the nematic order parameter, and ordered domains separated by lines of defects progressively grew and fused. This suggests that local cell-cell interactions drive the transition from disorder to order. To understand the mechanism of ordering, we perturbed the tissues physical constraints. We showed that while topology and geometry do not have a direct effect, anisotropic stretch biases the emerging orientation of the actin meshwork within hours. Surprisingly, although a Wnt protein gradient is expected to play a role in the actin ordering, the stretch-associated alignment happened without a Wnt enrichment. This demonstrates the role of tissue mechanics in the alignment of the actin fibers during the disorder-to-order transition.

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

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↗