Biology subjects

Bosveld, F.

Publications and source records attributed to Bosveld, F..

7 recordsLinked to original sources

bioRxiv2026

Tissue mechanics sets developmental scaling of collective cell migration

Despite substantial variation in adult size, animals within a species maintain consistent tissue patterns and shapes, a core property known as developmental scaling or size invariance. Developmental scaling has predominantly been attributed to the scaling of morphogen gradients and gene patterns to maintain positional information and cell fate specification1,2. However, development also necessitates collective cell flows that reshape tissues and reposition cells3,4. How these flows adapt to body size remains unclear. By combining quantitative live imaging, experimental perturbations, and physical modeling in the Drosophila thorax epithelium, we address this question in the context of a fundamental process: collective cell migration. We find that migration velocity scales linearly with tissue size, accounting for size-invariant cell positioning. While gene patterning scales with tissue size and modulates force generation, it is not sufficient to ensure proper velocity scaling. Instead, tissue mechanical properties govern the dependence of migration velocity on tissue size, enabling developmental scaling within the physiological range of animal sizes. These findings uncover principles and limits of size invariance by revealing how tissue mechanics sets the scaling behavior of collective cell flows with organismal size.

developmental biology↗

bioRxiv2026

Morphodynamic domains enable integration of live morphometrics and spatial transcriptomics

Tissue development emerges from the coordinated behaviors of thousands of cells, orchestrated by gene regulatory networks. Recent methodological advances now enable high-resolution live imaging of cell- and tissue-scale dynamics and the construction of spatially resolved gene expression atlases. However, quantitatively linking these modalities remains a central challenge, limiting our ability to understand how gene regulatory networks drive cell- and tissue-scale behaviors. Here, using the Drosophila thorax epithelium as a model system, we introduce an analytical and computational framework based on tissue morphodynamic domains: regions defined by coherent cell and tissue dynamics extracted from live imaging morphometrics. Integrating morphodynamic domains with spatial transcriptomics enables the inference of gene regulatory networks associated with distinct spatial cell- and tissue-level behaviors. Statistical cross-scale analyses further allow the interrogation and validation of gene function, confirming or revealing regulators of specific morphogenetic dynamics. In particular, our framework uncovers a role for the Toll-like receptor Tollo in modulating tissue flow, contraction, and apoptosis. Together, our work establishes a framework that integrates spatial transcriptomics with quantitative, multiscale live morphometrics, providing a generalizable strategy to probe and understand developmental processes.

developmental biology↗

bioRxiv2025

Tissue mechanics and systemic signaling safeguard epithelial tissue against spindle misorientation.

Multicellular organisms possess conserved safeguard mechanisms that ensure the maintenance of tissue integrity. Exploring these mechanisms has proven instrumental in understanding how tissues robustly develop and prevent tumor initiation. Here, we investigate how epithelial tissues preserve their architecture and cell number in the face of spindle mis-orientation. Spindle mis-orientation, due to the lack of spindle pulling forces, centrosomes, or mitotic rounding, can cause epithelial cells to be mispositioned within or outside the tissue, leading to significant cell loss. By inducing spindle mis-orientation in Drosophila epithelial tissue, we first found that acentrosomal microtubules and cell contractility prevent excessive epithelial cell loss by enabling mispositioned cells to reintegrate into the epithelium. However, this mechanism alone is insufficient to maintain the total epithelial cell number. We uncovered that epithelial mechanics and cell size sensing monitor and compensate for epithelial cell loss predominantly by reducing physiological apoptosis through Hippo/YAP signaling. Lastly, we found that systemic TNF signaling protects the organism by eliminating potentially harmful non-reintegrating cells. Overall, our results delineate the complementary roles of mechanics and systemic signaling in controlling cell number and position at both tissue and organismal levels.

developmental biology↗

bioRxiv2024

The Dystrophin-Dystroglycan complex ensures cytokinesis efficiency in Drosophila epithelia

Cytokinesis physically separates daughter cells at the end of cell division. This step is particularly challenging for epithelial cells, which are connected to their neighbors and to the extracellular matrix by transmembrane protein complexes. To systematically evaluate the impact of the cell adhesion machinery on epithelial cytokinesis efficiency, we performed an RNAi-based modifier screen in the Drosophila follicular epithelium. Strikingly, this unveiled adhesion molecules and transmembrane receptors that facilitate cytokinesis completion. Among these is Dystroglycan, which connects the extracellular matrix to the cytoskeleton via Dystrophin. Live imaging revealed that Dystrophin and Dystroglycan become enriched in the ingressing membrane, below the cytokinetic ring, during and after ring constriction. Using multiple alleles, including Dystrophin isoform-specific mutants, we show that Dystrophin/Dystroglycan localization is linked with unanticipated roles in regulating cytokinetic ring contraction and in preventing membrane regression during the abscission period. Altogether, we provide evidence that, rather than opposing cytokinesis completion, the machinery involved in cell-cell and cell-matrix interactions has also evolved functions to ensure cytokinesis efficiency in epithelial tissues.

cell biology↗

bioRxiv2022

Homeotic compartment curvature and tension control spatiotemporal folding dynamics.

Shape is a conspicuous and fundamental property of biological systems entailing the function of organs and tissues. While much emphasis has been put on how tissue tension and mechanical properties drive shape changes, whether and how a given tissue geometry influences subsequent morphogenesis remains poorly characterized. Here, we explored how curvature, a key descriptor of tissue geometry, impinges on the dynamics of epithelial tissue invagination. We found that the morphogenesis of the fold separating the adult Drosophila head and thorax segments is driven by the invagination of the Deformed (Dfd) homeotic compartment. Dfd controls invagination by modulating actomyosin organization and in-plane epithelial tension via the Tollo and Dystroglycan receptors. By experimentally introducing curvature heterogeneity within the homeotic compartment, we established that a curved tissue geometry converts the Dfd-dependent in-plane tension into an inward force driving folding. Accordingly, the interplay between in-plane tension and tissue curvature quantitatively explains the spatiotemporal folding dynamics. Collectively, our work highlights how genetic patterning and tissue geometry provide a simple design principle driving folding morphogenesis during development.

developmental biology↗

bioRxiv2021

Multi-view confocal microscopy enables multiple organ and whole organism live-imaging

Understanding how development is coordinated in multiple tissues and gives rise to fully functional organs or whole organisms necessitates microscopy tools. Over the last decade numerous advances have been made in live-imaging, enabling high resolution imaging of whole organisms at cellular resolution. Yet, these advances mainly rely on mounting the specimen in agarose or aqueous solutions, precluding imaging of organisms whose oxygen uptake depends on ventilation. Here, we implemented a multi-view multi-scale microscopy strategy based on confocal spinning disk microscopy, called Multi-View confocal microScopy (MuViScopy). MuViScopy enables live-imaging of multiple organs with cellular resolution using sample rotation and confocal imaging without the need of sample embedding. We illustrate the capacity of MuViScopy by live-imaging Drosophila melanogaster pupal development throughout metamorphosis, highlighting how internal organs are formed and multiple organ development is coordinated. We foresee that MuViScopy will open the path to better understand developmental processes at the whole organism scale in living systems that necessitates gas exchange by ventilation.

developmental biology↗

bioRxiv2018

Tricellular junction proteins promote disentanglement of daughter and neighbour cells during epithelial cytokinesis

In epithelial tissue, new cell-cell junctions are formed upon cytokinesis. To understand junction formation during cytokinesis, we explored in Drosophila epithelium, de novo formation of tricellular septate junctions (TCJs). We found that upon midbody formation, the membranes of the two daughter cells and of the neighbouring cells located below the adherens junction (AJ) remain entangled in a 4-cell structure apposed to the midbody. The septate junction protein Discs-Large and components of the TCJ, Gliotactin and Anakonda accumulate in this 4-cell structure. Subsequently, a basal movement of the midbody parallels the detachment of the neighbouring cell membranes from the midbody, the disengagement of the daughter cells from their neighbours and the reorganisation of TCJs between the two daughter cells and their neighbouring cells. While the movement of midbody is independent of the Alix and Shrub abscission regulators, the loss of Gliotactin or Anakonda function impedes both the resolution of the connection between the daughter-neighbour cells and midbody movement. TCJ proteins therefore control an additional step of cytokinesis necessary for the disentanglement of the daughter cells and their neighbours during cytokinesis.

developmental biology↗