Biology subjects

Rios-Barrera, L. D.

Publications and source records attributed to Rios-Barrera, L. D..

4 recordsLinked to original sources

bioRxiv2025

Adhesion to a common ECM mediates interdependence in tissue morphogenesis in Drosophila

For organs to be functional, the cells and tissues that constitute them must effectively interact with each other and coordinate their behaviours. Halfway during Drosophila embryogenesis, two lateral epidermal sheets stretch to fuse at the dorsal midline; concomitant with this, the main tubes of the respiratory system also shift dorsally. Here, we show that these processes occur simultaneously and are coordinated by the adhesion of the epidermal sheets and a subset of cells of the tracheal trunks to a common extracellular matrix (ECM) that separates them. We show that during dorsal closure, tracheal trunk cells extend protrusions towards the ECM underneath the epidermis. These protrusions are under tension, suggesting they have a mechanical function. Additionally, perturbing adhesion between tracheal cells and the epidermis affects the development of both tissues. Altogether, our findings uncover a novel mechanism used for tissue coordination during development, one that is based on tissue adhesion towards a common ECM capable of transmitting forces across the embryo.

developmental biology↗

bioRxiv2021

Subcellular tube guidance requires anchoring of the apical and basal actin cortices through late endosomes

The subcellular membrane-trafficking system plays many roles in cell growth and morphogenesis, from bulk membrane provision to targeted delivery of membrane proteins and other cargos. In tracheal terminal cells of the Drosophila respiratory system, endocytosis and trafficking through late endosomes balances membrane delivery between the basal plasma membrane and the apical membrane that forms a subcellular tube, but it has been unclear how the direction of growth of the subcellular tube with the overall growth of the cell is coordinated. We show here that endosomes are involved in this process as coordinators of F-actin. Actin assembles around late endocytic vesicles in the growth cone of the cell, reaching from the tip of the subcellular tube to the leading filopodia of the basal membrane. Preventing actin nucleation at late endosomes disturbs the directionality of tube growth, uncoupling it from the direction of cell elongation. Severing actin in this area affects tube integrity. Our findings show a new role for late endosomes in directing cell morphogenesis by organizing actin, in addition to their known role in membrane and protein trafficking.

cell biology↗

bioRxiv2020

Transcytosis via the late endocytic pathway as a cell morphogenetic mechanism

Plasma membranes fulfil many physiological functions. In polarized cells, different membrane compartments take on specialized roles, each being allocated correct amounts of membrane. The Drosophila tracheal system, an established tubulogenesis model, contains branched terminal cells with subcellular tubes formed by apical plasma membrane invagination. We show that apical endocytosis and late endosome-mediated trafficking determine the membrane allocation to the apical and basal membrane domains. Basal plasma membrane growth stops if endocytosis is blocked, whereas the apical membrane grows excessively. Plasma membrane is initially delivered apically, and then continuously endocytosed, together with apical and basal cargo. We describe an organelle carrying markers of late endosomes and multivesicular bodies (MVBs) that is abolished by inhibiting endocytosis, and which we suggest acts as transit station for membrane destined to be redistributed both apically and basally. This is based on the observation that disrupting MVB formation prevents growth of both compartments.

cell biology↗

bioRxiv2017

Dual Function For Tango1 In Secretion Of Bulky Cargo And In ER-Golgi Morphology

Tango1 helps the efficient delivery of large proteins to the cell surface. We show here that loss of Tango1, in addition to interfering with protein secretion, causes ER stress and defects in cell and ER/Golgi morphology. We find that the previously observed dependence of smaller cargos on Tango1 is a secondary effect, due to an indirect requirement: if large cargos like Dumpy, which we identify here as a new Tango1 cargo, are removed from the cell, non-bulky proteins re-enter the secretory pathway. Removal of the blocking cargo also attenuates the ER-stress response, and cell morphology is restored. Thus, failures in the secretion of non-bulky proteins, ER stress and defective cell morphology are secondary consequences of the retention of cargo. By contrast, the ERES defects in Tango1-depleted cells persist in the absence of bulky cargo, showing that they are due to a secretion-independent function of Tango1. Therefore, the maintenance of proper ERES architecture may be a primary function for Tango1.

cell biology↗