Biology subjects

Alegot, H.

Publications and source records attributed to Alegot, H..

5 recordsLinked to original sources

bioRxiv2024

Biom3d, a modular framework to host and develop 3D segmentation methods

U-Net is a convolutional neural network model developed in 2015 and has proven to be one of the most inspiring deep-learning models for image segmentation. Numerous U-Net-based applications have since emerged, constituting a heterogeneous set of tools that illustrate the current reproducibility crisis in the deep-learning field and that remain slow to spread in application fields such as 3D bioimaging. Here we propose a solution named Biom3d, a modular deep learning framework facilitating the integration and development of novel models, metrics, or training schemes for 3D image segmentation. The development philosophy of Biom3d provides an improved code sustainability and reproducibility in line with the FAIR principles and is available as a graphical user interface and an open-source deep-learning framework to target a large community of users, from end users to deep learning developers.

bioinformatics↗

bioRxiv2024

Tricellular junction recruitment of the Wave regulatory complex by Sidekick and Lar induces protrusive activity resolving cell intercalation

Cell intercalation, a fundamental morphogenetic process characterized by the exchange of neighboring cells, plays a pivotal role in epithelial tissue development. While the initiation of new junctions remains poorly understood, recent research indicates the involvement of tricellular junction actors. In this study, we explore the contribution of the WAVE regulatory complex (WRC), a critical regulator of branched F-Actin generation, in tissue elongation and cell intercalation within the Drosophila ovarian follicular epithelium. WRC localizes at tricellular junctions, where it orchestrates the generation of highly dynamic protrusions emanating from one cell and extending between the bicellular junctions of neighboring cells. This protrusive activity is essential for the initiation of new junctions in cells located at the extremities of these junctions. Furthermore, our findings indicate that WRC recruitment at tricellular junctions is a redundant process, involving the cooperative action of the two transmembrane proteins Sidekick and Lar. Disruption of this recruitment impairs protrusive activity, cell intercalation resolution, and tissue elongation, thereby mechanistically bridging molecular, cellular and tissular scales. Consequently, this elucidates a critical mechanism underlying epithelial morphogenesis through actin polymerization at tricellular junctions.

cell 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↗

bioRxiv2019

Oriented basement membrane fibrils provide a memory for F-actin planar polarization via the Dystrophin-Dystroglycan complex during tissue elongation

How extracellular matrix participates to tissue morphogenesis is still an open question. In the Drosophila ovarian follicle, it has been proposed that after Fat2-dependent planar polarization of the follicle cell basal domain, oriented basement membrane (BM) fibrils and F-actin stress fibers constrain follicle growth, promoting its axial elongation. However, the relationship between BM fibrils and stress fibers and their respective impact on elongation are unclear. We found that Dystroglycan (Dg) and Dystrophin (Dys) are involved in BM fibril deposition. Moreover, they orient stress fibers, by acting locally and in parallel to Fat2. Nonetheless, Dg-Dys complex-mediated cell autonomous control of F-actin fibers orientation relies on the previous BM fibril deposition, indicating two distinct but interdependent functions. Thus, the Dg-Dys complex works as a critical organizer of the epithelial basal domain, regulating both F-actin and BM. Furthermore, BM fibrils act as a persistent cue for the orientation of stress fibers that are the main effector of elongation.

developmental biology↗

bioRxiv2017

Jak-Stat pathway induces Drosophila follicle elongation by a gradient of apical contractility

Tissue elongation and its control by spatiotemporal signals is a major developmental question. Currently, it is thought that Drosophila ovarian follicular epithelium elongation requires the planar polarization of the basal domain cytoskeleton and of the extra-cellular matrix, associated with a dynamic process of rotation around the anteroposterior axis. Here we show, by careful kinetic analysis of fat2 mutants, that neither basal planar polarization nor rotation is required during a first phase of follicle elongation. Conversely, a JAK-STAT signaling gradient from each follicle pole orients early elongation. JAK-STAT controls apical pulsatile contractions, and Myosin II activity inhibition affects both pulses and early elongation. Early elongation is associated with apical constriction at the poles and oriented cell rearrangements, but without any visible planar cell polarization of the apical domain. Thus, a morphogen gradient can trigger tissue elongation via a control of cell pulsing and without planar cell polarity requirement.\n\nImpact StatementFollicle elongation does not rely solely on the basal side of the cells but also requires a mechanism integrating a developmental cue with a morphogenetic process involving their apical domain.

developmental biology↗