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© Romain Levayer, Institut Pasteur
Epithelial layer of the Drosophila pupal thorax (notum). White : cell contour (E-cadherin), pseudocolour : Dpp sensor.
Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Developmental cell - 21 Jun 2021

Valon L, Davidović A, Levillayer F, Villars A, Chouly M, Cerqueira-Campos F, Levayer R,

Link to Pubmed [PMID] – 34081909

Link to HAL – Click here

Link to DOI – S1534-5807(21)00435-410.1016/j.devcel.2021.05.006

Dev Cell 2021 06; 56(12): 1700-1711.e8

What regulates the spatiotemporal distribution of cell elimination in tissues remains largely unknown. This is particularly relevant for epithelia with high rates of cell elimination where simultaneous death of neighboring cells could impair epithelial sealing. Here, using the Drosophila pupal notum (a single-layer epithelium) and a new optogenetic tool to trigger caspase activation and cell extrusion, we first showed that death of clusters of at least three cells impaired epithelial sealing; yet, such clusters were almost never observed in vivo. Accordingly, statistical analysis and simulations of cell death distribution highlighted a transient and local protective phase occurring near every cell death. This protection is driven by a transient activation of ERK in cells neighboring extruding cells, which inhibits caspase activation and prevents elimination of cells in clusters. This suggests that the robustness of epithelia with high rates of cell elimination is an emerging property of local ERK feedback.