Biology subjects

Andrieu, C.

Publications and source records attributed to Andrieu, C..

5 recordsLinked to original sources

bioRxiv2026

Development of a stable microbial community for the study of plasmid-mediated antimicrobial resistance in a continuous culturing device

Horizontal gene transfer (HGT) is a major contributor to the spread of antimicrobial resistance (AMR) in microbial communities, particularly through conjugative plasmids. The dynamics of the spread of these plasmids in a susceptible microbial community requires a defined and controllable in vitro system, which is currently lacking from existing laboratory evolution systems. Here we describe the development of TriComm, an engineered microbial community of three strains with complementary amino acid auxotrophies, maintained in continuous culture under real-time optical and fluorescence monitoring. We show that two conjugative plasmids carrying resistance genes (blaOXA-48 and mcr-1) generally rescued TriComm from collapse under antimicrobial treatment, and that this protection was dependent on conjugative transfer. Community composition remained stable across most conditions, including after the AMR plasmid had spread through the population. Through mathematical modeling we predict that modulating both drug efficacy and conjugation rate can lead to the collapse of the community, suggesting potential strategies to limit the spread of AMR via HGT.

microbiology↗

bioRxiv2025

Cell exit during EMT is mechanically triggered independently of E-Cadherin loss

Epithelial-to-mesenchymal transition (EMT) is a fundamental cell process with essential functions in tissue and organ formation during development but also metastasis during cancer progression. The shift between these two states is driven by evolutionary conserved transcription factors. Cell exit from the epithelium of origin is considered to be a mere consequence of progressive adhesion loss due to transcriptional repression of genes encoding molecules such as E-Cadherin or cell polarity regulators. Here we show in the Drosophila leg that, counterintuitively, adhesions (as well as cell polarity) are maintained during cell exit, while an apico-basal force is applied on E-Cadherin complexes in vivo. By combining a genetic screen, optogenetics and laser ablation experiments, we found that this pulling force originates from transient basal filopodia-like protrusions, formed as soon as cells start to exit. Finally, apical cell detachment requires -Spectrin activity, suggesting that the lateral cortex is required to efficiently transmit basal forces up to the apical cell pole. Our results indicate that, in a mature tissue, cell exit during EMT is a mechanically controlled process. Such a mechanism driving EMT without of E-Cadherin loss could fuel metastatic dissemination of collectively migrating cancer cells.

developmental biology↗

bioRxiv2025

Apical-basal polarity regulates Collagen IV-dependent cell-cell adhesion in the Drosophila adipose tissue

E-Cadherin-based adherens junctions are the main type of junctional compartment in epithelia mediating cell-cell adhesion. The apical-basal cell polarity machinery positions adherens junctions at the apical-lateral border. The Drosophila adipose tissue, called the fat body, forms a monolayer in which cells adhere to each other through the binding of Integrin to pericellular Collagen IV concentrations. It is currently not known, how these atypical adhesion complexes form. Here we examine the epithelial apical-basal cell polarity network in the larval fat body. We find that this tissue displays an apical-basal cell polarity, with the apical proteins aPKC, Crumbs and Par-6 and the basolateral proteins Lgl and Dlg on opposite sides. Crumbs, aPKC, Scribble, and Lgl knockdown in the fat body leads to cell-cell-adhesion defects. We find that aPKC plays a key role in mediating cell-cell adhesion by regulating the formation of Collagen IV-Intercellular-Adhesion-Concentrations. We further show that during fat body remodeling, the steroid hormone Ecdysone regulates the loss of apical-basal polarity and Collagen IV-Intercellular-Adhesion-Concentrations to induce cell-cell dissociation and initiation of amoeboid swimming cell migration. Our work hence uncovers a novel role for the apical-basal polarity machinery in the Drosophila adipose tissue in regulating cell-cell adhesion via Collagen IV-Intercellular-Adhesion-Concentrations.

developmental biology↗

bioRxiv2024

Cell deformations generated by dynamic cortical actin waves drive in vivo swimming migration

Amoeboid cell migration drives many important developmental and disease-related processes including immune responses and cancer metastasis. Swimming cell migration is a subtype of amoeboid migration observed in cells in suspension ex vivo. However, the mechanism underlying swimming migration in vivo under physiological conditions is unknown. Using Drosophila fat body cells (FBCs) as a model, we show that FBCs actively swim to patrol the pupa. Their stop-and-go random walk is powered through the generation of oscillatory actomyosin waves, rather than persistent actin flows used by cells swimming in vitro. These actomyosin waves exert peristaltic compressive forces as they move to the cell rear. This causes cell elongation towards the front to propel the cell forward. In addition, we demonstrate that, unlike in other types of amoeboid migration, all three RhoGTPases, RhoA, Cdc42 and Rac1, are required for FBC migration. They control actin wave formation by regulating actin polymerisation through the formin Dia. Furthermore, RhoA at the cell rear induces actomyosin contractions via Rho kinase and myosin II to generate cell deformations. Importantly, our work reveals that swimming migration is a novel in vivo migration mode for rapid and long-range cell dispersal, potentially also used by other cells such as immune cells and cancer cells when encountering an aqueous environment.

cell biology↗

bioRxiv2018

Basolateral localization of MMP14 drives apicobasal polarity change during EMT independently of its catalytic activity

The transmembrane Matrix Metalloproteinase MMP14/MT1-MMP is known to promote cell migration by cleavage of the extracellular matrix. To initiate migration, epithelial cells need to gain mesenchymal attributes. They reduce cell-cell junctions and apicobasal polarity and gain migratory capabilities. This process is named epithelial-mesenchymal transition (EMT). MMP14s implication in EMT is still ill-defined. We used chick neural crest (NC) cells as a model to explore the function of MMP14 in physiological EMT. Our results show that MMP14 is expressed by chick NC cells. However, it is its subcellular localization, rather than its expression, that correlates with EMT. MMP14 is first apical and switches to basolateral domains during EMT. Loss of function and rescue experiments show that MMP14 is involved in EMT independently of its catalytic activity. It lies downstream of pro-EMT genes and upstream of cell polarity. We found that basolateral localization of MMP14 is required and sufficient to induce polarity change in NC cells and neuroepithelial cells, respectively. These effects on polarity occur without impact on cell-cell adhesion or the extracellular matrix. Overall, our data points to a new function of MMP14 in EMT that will need to be further explored in other systems such as cancer cells.

developmental biology↗