Developmental delay ensures global tissue size robustness upon local induction of apoptosis DOI Creative Commons
Ralitza Staneva,

Gabriel Sobczyk-Moran,

Florence Levillayer

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 21, 2024

Abstract The capacity of our tissues to cope with external and internal stress relies on the tight coupling between cell proliferation, growth death. This is assumed be based compensatory where local mitogenic signals mechanical inputs generated by dying cells promote neighbouring proliferation. However, proliferation was mostly studied in context massive death induction, irradiation, surgical tissue ablation or upon genetic perturbation apoptosis execution. It remains thus unclear whether same mechanism operates during physiological programmed mild induction apoptosis, especially vivo . Here, we use Drosophila prospective wing (the larval disc), study impact size pattern. We first confirmed that could recover its final compensate for apoptosis. using spatial statistics found surprisingly not associated any increase it clonal compartment Compensation driven instead a JNK dependant delay lengthening stage which required reach target size. These results suggest compensation here global response rather induction. Accordingly, while total maintained despite this fails correct reduction number, hence modulating shape proportion. Overall, opens novel perspectives regulation outlines context-dependency mechanisms.

Language: Английский

Live imaging of airway epithelium reveals that mucociliary clearance modulates SARS-CoV-2 spread DOI Creative Commons
Mark E. Becker, Laura Martin‐Sancho, Lacy M. Simons

et al.

Nature Communications, Journal Year: 2024, Volume and Issue: 15(1)

Published: Nov. 2, 2024

SARS-CoV-2 initiates infection in the conducting airways, where mucociliary clearance inhibits pathogen penetration. However, it is unclear how impacts spread after established. To investigate viral at this site, we perform live imaging of infected differentiated primary human bronchial epithelium cultures for up to 12 days. Using a fluorescent reporter virus and markers cilia mucus, longitudinally monitor mucus motion, ciliary infection. Infected cell numbers peak 4 days post infection, forming characteristic foci that tracked movement. Inhibition MCC using physical genetic perturbations limits foci. Later deteriorates. Increased secretion accompanies motion defects, but vectorial resume removal, suggesting may mediate deterioration. Our work shows while can facilitate initial subsequent decreases inhibit spread, revealing complex interplay between MCC.

Language: Английский

Citations

4
Epithelial cell extrusion at a glance DOI Creative Commons

Aline Grata,

Romain Levayer

Journal of Cell Science, Journal Year: 2025, Volume and Issue: 138(8)

Published: April 15, 2025

ABSTRACT The robustness and plasticity of epithelial tissues rely on the capacity such to eliminate cells without affecting their sealing. This is achieved by cell extrusion – a well-orchestrated series remodelling steps involving eliminated its neighbours which ensures constant maintenance mechanical chemical barrier properties while allowing expulsion. In this Cell Science at Glance accompanying poster, we describe that take place within dying or extruding cells, as well neighbouring outlining commonalities variations between organisms. These include reorganization cytoskeleton cell–cell junctions alters contribution coupling mechanotransduction. We also discuss larger-scale coordination tissue morphogenesis, surveillance mechanisms, pathologies cancer chronic inflammation. Altogether, outline complexity minimalist morphogenetic process.

Language: Английский

Citations

0
Role of tight junction proteins in shaping the immune milieu of malignancies DOI

Laxmi Kumari,

Reena Yadav, Yashwant Kumar

et al.

Expert Review of Clinical Immunology, Journal Year: 2024, Volume and Issue: 20(11), P. 1305 - 1321

Published: Aug. 10, 2024

Introduction Tight junctions (TJs) and their constituent proteins play pivotal roles in cellular physiology anatomy by establishing functional boundaries within between neighboring cells. While the involvement of TJ proteins, such as claudins, cancer is extensively studied, studies highlighting interaction with immune system are still meager. Studies indicate that alterations cytokines cell populations can affect compromising barrier function exacerbating pro-inflammatory conditions, potentially leading to epithelial malignancy. Disrupted TJs established tumors may foster a pro-tumor microenvironment, facilitating tumor progression, invasion, epithelial-to-mesenchymal transition metastasis. Although previous literature contains many describing pathogenesis malignancies role modulating microenvironment just beginning be unleashed.

Language: Английский

Citations

2
The directionality of collective cell delamination is governed by tissue architecture and cell adhesion in a Drosophila carcinoma model DOI Creative Commons
Marta Mira-Osuna, Steffen Plunder, Eric Théveneau

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 10, 2024

Abstract Carcinomas originate in epithelia and are the most frequent type of cancers. Tumor progression starts with collective delamination live tumors out epithelium, requires modulation cell adhesion. Yet, it remains elusive exactly how remodeling epithelial cell-cell cell-extracellular matrix contacts contribute to metastasis onset directionality. We used Drosophila melanogaster larval eye disc study cooperative oncogenesis determine contribution bi- tricellular septate junction (SJ) components tumor flat pseudostratified epithelia. reveal that loss-of-function alone can promote death whereas synergic interaction oncogenic Ras triggers living tumorigenic cells. Spatiotemporal analyses apical basal processes differ terms identity, polarity cell-ECM contacts. Using a combination vivo silico approaches, we report SJ-depleted V12 trigger tissue folding or regardless order which remodeled. In striking contrast, formed flat, squamous epithelia, first undergo constriction acquire dome-like shape. Tumors enriched adhesion molecules form an neck at interface contact between mutant cells wild-type neighbors. Concomitant cytoskeleton remodeling, emit protrusions lumen progressively delaminate through while remaining cohesive. Our reveals architecture changes drive directionality neoplastic epithelium.

Language: Английский

Citations

0
Developmental delay ensures global tissue size robustness upon local induction of apoptosis DOI Creative Commons
Ralitza Staneva,

Gabriel Sobczyk-Moran,

Florence Levillayer

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 21, 2024

Abstract The capacity of our tissues to cope with external and internal stress relies on the tight coupling between cell proliferation, growth death. This is assumed be based compensatory where local mitogenic signals mechanical inputs generated by dying cells promote neighbouring proliferation. However, proliferation was mostly studied in context massive death induction, irradiation, surgical tissue ablation or upon genetic perturbation apoptosis execution. It remains thus unclear whether same mechanism operates during physiological programmed mild induction apoptosis, especially vivo . Here, we use Drosophila prospective wing (the larval disc), study impact size pattern. We first confirmed that could recover its final compensate for apoptosis. using spatial statistics found surprisingly not associated any increase it clonal compartment Compensation driven instead a JNK dependant delay lengthening stage which required reach target size. These results suggest compensation here global response rather induction. Accordingly, while total maintained despite this fails correct reduction number, hence modulating shape proportion. Overall, opens novel perspectives regulation outlines context-dependency mechanisms.

Language: Английский

Citations

0