Summary of ssbd-repos-000272


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DOI
Title
Epidermal growth factor receptor signaling protects epithelia from morphogenetic instability and tissue damage in Drosophila
Description

Original image data of the manuscript by Yoshida and Hayashi (in press, preprint available https://doi.org/10.1101/2022.08.28.505615).

Submited Date
2023-02-21
Release Date
2023-03-09
Updated Date
-
License
Data size
146.3 GB
Data formats
Oib (raw data) or TIFF files of multi channel confocal images.

Organism
Drosophila melanogaster
Strain
-
Cell Line
-
Molecular Function (MF)
-
Biological Process (BP)
-
Cellular Component (CC)
-
Study Type
-
Imaging Methods
-

Method Summary

Described in the manuscript.

Related paper(s)

Yoshida, Kentaro, Hayashi, Shigeo (2022/01/01), Epidermal growth factor receptor signaling protects epithelia from morphogenetic instability and tissue damage in <em>Drosophila</em>, 2022.08.28.505615

Published in Aug. 22, 2022

(Abstract) Dying cells in the epithelia communicate with neighboring cells to initiate coordinated cell removal to maintain epithelial integrity. Naturally occurring apoptotic cells are mostly extruded basally and engulfed by macrophages. Here, we investigated the role of Epidermal growth factor (EGF) receptor (EGFR) signaling in the maintenance of epithelial homeostasis. In Drosophila embryos, epithelial tissues undergoing groove formation preferentially enhanced extracellular signal-regulated kinases (ERK) signaling. In EGFR mutant embryos at stage 11, sporadic apical cell extrusion in the head initiates a cascade of apical extrusions of apoptotic and non-apoptotic cells that sweeps the entire ventral body wall. Here, we showed that clustered apoptosis, groove formation, and wounding sensitized EGFR mutant epithelia to initiate massive tissue disintegration. We further showed that tissue detachment from the vitelline membrane, which frequently occurs during morphogenetic processes, is a key trigger for the EGFR mutant phenotype. These findings indicate that, in addition to cell survival, EGFR plays a role in maintaining epithelial integrity, which is essential for protecting tissues from transient instability caused by morphogenetic movement and damage.Competing Interest StatementThe authors have declared no competing interest.
Related paper(s)

Kentaro Yoshida, Shigeo Hayashi (2023) Epidermal growth factor receptor signaling protects epithelia from morphogenetic instability and tissue damage in Drosophila., Development (Cambridge, England), Volume 150, Number 5

Published in 2023 Mar 1 (Electronic publication in March 9, 2023, midnight )

(Abstract) Dying cells in the epithelia communicate with neighboring cells to initiate coordinated cell removal to maintain epithelial integrity. Naturally occurring apoptotic cells are mostly extruded basally and engulfed by macrophages. Here, we have investigated the role of Epidermal growth factor (EGF) receptor (EGFR) signaling in the maintenance of epithelial homeostasis. In Drosophila embryos, epithelial tissues undergoing groove formation preferentially enhanced extracellular signal-regulated kinase (ERK) signaling. In EGFR mutant embryos at stage 11, sporadic apical cell extrusion in the head initiates a cascade of apical extrusions of apoptotic and non-apoptotic cells that sweeps the entire ventral body wall. Here, we show that this process is apoptosis dependent, and clustered apoptosis, groove formation, and wounding sensitize EGFR mutant epithelia to initiate massive tissue disintegration. We further show that tissue detachment from the vitelline membrane, which frequently occurs during morphogenetic processes, is a key trigger for the EGFR mutant phenotype. These findings indicate that, in addition to cell survival, EGFR plays a role in maintaining epithelial integrity, which is essential for protecting tissues from transient instability caused by morphogenetic movement and damage.
(MeSH Terms)

Contact(s)
Shigeo Hayashi
Organization(s)
RIKEN , Center for Biosystems Dynamics Research , Laboratory for Morphogenetic Signaling
Image Data Contributors
Kentaro Yoshida
Quantitative Data Contributors

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