Biology subjects

Matamoro-Vidal, A.

Publications and source records attributed to Matamoro-Vidal, A..

5 recordsLinked to original sources

bioRxiv2025

Interfacial tension and growth both contribute to mechanical cell competition

Tissue plasticity and homeostasis rely on the mutual interplay between cell behaviour and mechanical inputs1. Yet, mechanical stress can also contribute to the evolution of some pathologies, notably by accelerating pretumoural cell expansion through the process of mechanical cell competition2-5. Mechanical cell competition is a conserved process in which one cell population is preferentially eliminated when mixed with another cell population due to its higher sensitivity to mechanical stress2,3,5-8. Most of the recent theoretical and experimental explorations of mechanical cell competition focused so far on the contribution of growth and pressure to cell elimination and were limited to few genetic contexts, including the activation of Ras in vivo2,8, and the mutation of the polarity gene scribble in mammalian cell culture3,4,9. However, it remains unclear whether other oncogenes can trigger similar mechanisms and whether growth is generally the only central regulator of cell compaction and cell elimination. Using the Drosophila pupal notum (a single layer epithelium), quantitative live imaging and vertex modelling, we revisited the mechanisms contributing to cell compaction and cell elimination during mechanical cell competition. Doing so, we outlined the co-existence of two modes of wild type (WT) cell compaction near oncogenic cells, namely the compaction driven by growth versus local compaction driven by increased tension at tumoural/WT cell interfaces in zones of high curvature (similar to "Laplace pressure"). We highlighted distinctive signatures in cell deformation and cell elimination distribution that can delineate these two modes of compaction, and we recapitulated them in silico and in vivo using genetic backgrounds affecting growth and/or interfacial tension independently. Altogether, this study reveals for the first time the contribution of interfacial tension-driven compaction to mechanical cell competition and outlines the co-existence of various modes of compaction during cell elimination and pretumoural clone expansion.

cell biology↗

bioRxiv2022

Patterned apoptosis modulates local growth and tissue shape in a fast-growing epithelium

What regulates organ size and shape remains one of the fundamental mysteries of modern biology. So far, research in this area has primarily focused on deciphering the regulation in time and space of growth and cell division, while the contribution of cell death has been much more neglected. This includes studies of the Drosophila wing imaginal disc, the prospective fly wing which undergoes massive growth during larval stage, and represents one of the best characterised systems for the study of growth and patterning. So far, it has been assumed that cell death was relatively neglectable in this tissue and as a result the pattern of growth was usually attributed to the distribution of cell division. Here, using systematic mapping and registration combined with quantitative assessment of clone size and disappearance, we show for the first time that cell death is not neglectable, and outline a persistent pattern of cell death and clone elimination in the disc. Local variation of cell death is associated with local variation of clone size, pointing to an impact of cell death on local growth which is not fully compensated by proliferation. Using morphometric analyses of adult wing shape and genetic perturbations, we provide evidence that patterned death affects locally and globally adult wing shape and size. This study describes a roadmap for accurate assessment of the contribution of cell death to tissue shape, and outlines for the first time an important instructive role of cell death in modulating quantitatively local growth and the morphogenesis of a fast-growing tissue.

developmental biology↗

bioRxiv2021

Microtubule disassembly by caspases is the rate-limiting step of cell extrusion

Epithelial cell death is essential for tissue homeostasis, robustness and morphogenesis. The expulsion of epithelial cells following caspase activation requires well-orchestrated remodeling steps leading to cell elimination without impairing tissue sealing. While numerous studies have provided insight about the process of cell extrusion, we still know very little about the relationship between caspase activation and the remodeling steps of cell extrusion. Moreover, most studies of cell extrusion focused on the regulation of actomyosin and steps leading to the formation of a supracellular contractile ring. However, the contribution of other cellular factors to cell extrusion has been poorly explored. Using the Drosophila pupal notum, a single layer epithelium where most extrusion events are caspase-dependent, we first showed that the initiation of cell extrusion and apical constriction are surprisingly not associated with the modulation of actomyosin concentration/dynamics. Instead, cell apical constriction is initiated by the disassembly of a medio-apical mesh of microtubules which is driven by effector caspases. We confirmed that local and rapid increase/decrease of microtubules is sufficient to respectively expand/constrict cell apical area. Importantly, the depletion of microtubules is sufficient to bypass the requirement of caspases for cell extrusion. This study shows that microtubules disassembly by caspases is a key rate-limiting steps of extrusion, and outlines a more general function of microtubules in epithelial cell shape stabilisation.

cell biology↗

bioRxiv2018

Robustness of bristle number to temperature and genetic background varies with bristle type and is regulated by miR-9a.

Robustness is the invariance of a given phenotype when faced with a given incoming genetic or environmental variation. Such essential property is being studied in a wide diversity of traits in many organisms but it is difficult to compare the results obtained on the robustness of different traits with each other given the differences that exist between traits in the way they are measured, in their genetic architecture and development. In this study, we assessed robustness of bristle number to incoming genetic and environmental variation for eight bristle types in the fruit fly Drosophila melanogaster, allowing for a straightforward comparison of the robustness observed between bristle types. We measured the response of bristle number mean and variance to changes in temperature and in the number of copies of two genes (scute and miR-9a) known to be involved in bristle development. Many combinations between the three factors were tested, thus allowing to test for the effect of each factor in different contexts for the two other factors - to which we refer herein as different backgrounds. We have found different responses between bristle types, suggesting that they present different levels of robustness to the factors tested. In addition, we have found that temperature and miR-9a affect more generally the variance of the traits rather than their means, thus fulfilling a criteria usually admitted to identify robustness factors.

genetics↗

bioRxiv2017

Quantitative morphological variation in the developing Drosophila wing

Quantitative variation in morphology is pervasive in all species and is the basis for the evolution of differences among species. The developmental causes of such variation are a relatively neglected research topic. Quantitative comparisons of variation arising at different developmental stages with the variation in the final structure enable us to determine when variation arises, and to generate hypotheses about the causes of that variation. We measured shape and size variation in the wing of Drosophila melanogaster at three developmental stages: late third instar, post-pupariation and in the adult fly. Flies of a wild-type and two mutants (shf and ds) with effects on the adult wing shape and size were studied. Despite experimental noise related to the difficulty of comparing developing structures, we found consistent differences in wing shape and size at each developmental stage between genotypes. In addition we provide linear rules allowing to link late disc morphology with early wings. Our approach provides a framework to analyze quantitative morphological variation in the developing fly wing. This framework should help to characterize the natural variation of the larval and pupal wing shape, and to measure the contribution of the processes occurring during these developmental stages to the natural variation in adult wing morphology.

genetics↗