Reduction of endocytosis and EGFR signaling is associated with the switch from isolated to clustered apoptosis during epithelial tissue remodeling in Drosophila

Yuswan, Kevin; Sun, Xiaofei; Kuranaga, Erina et al.

PLoS Biology, 2024, 22(10), e3002823

Number of Access:297（2025-09-03 17:26 Counts）

Identifier to cite or link to this item: https://hdl.handle.net/11094/98358

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Title
Reduction of endocytosis and EGFR signaling is associated with the switch from isolated to clustered apoptosis during epithelial tissue remodeling in Drosophila
Creator
CreatorName
Yuswan, Kevin
CreatorName
Sun, Xiaofei
NRID
1000090376591 1000090376591
CreatorName
Kuranaga, Erina
ORCID
0000-0002-1916-6903 0000-0002-1916-6903
researchmap permalink
7000022447 7000022447
NRID
1000060620474 1000060620474
Scopus Author ID
10341169200 10341169200
CreatorName
Umetsu, Daiki
Description
Yuswan K., Sun X., Kuranaga E., et al. (2024) Reduction of endocytosis and EGFR signaling is associated with the switch from isolated to clustered apoptosis during epithelial tissue remodeling in Drosophila. PLoS Biology 22(10), e3002823. doi.org/10.1371/journal.pbio.3002823.
Abstract
Epithelial tissues undergo cell turnover both during development : and for homeostatic maintenance. Removal of cells is coordinated with the increase in number of newly dividing cells to maintain barrier function of the tissue. In Drosophila metamorphosis, larval epidermal cells (LECs) are replaced by adult precursor cells called histoblasts. Removal of LECs must counterbalance the exponentially increasing adult histoblasts. Previous work showed that the LEC removal accelerates as endocytic activity decreases throughout all LECs. Here, we show that the acceleration is accompanied by a mode switching from isolated single-cell apoptosis to clustered ones induced by the endocytic activity reduction. We identify the epidermal growth factor receptor (EGFR) pathway via extracellular-signal regulated kinase (ERK) activity as the main components downstream of endocytic activity in LECs. The reduced ERK activity, caused by the decrease in endocytic activity, is responsible for the apoptotic mode switching. Initially, ERK is transiently activated in normal LECs surrounding a single apoptotic LEC in a ligand-dependent manner, preventing clustered cell death. Following the reduction of endocytic activity, LEC apoptosis events do not provoke these transient ERK up-regulations, resulting in the acceleration of the cell elimination rate by frequent clustered apoptosis. These findings contrasted with the common perspective that clustered apoptosis is disadvantageous. Instead, switching to clustered apoptosis is required to accommodate the growth of neighboring tissues.
Publisher
Public Library of Science
Source Title
PLoS Biology
Volume (Issue)
22(10)
Page
e3002823
Date of Issued
2024-10-14
Language
English
Handle URL
https://hdl.handle.net/11094/98358
PISSN
15449173
eISSN
15457885
Relation.isIdenticalTo
DOI (Publisher Version)
https://doi.org/10.1371/journal.pbio.3002823
Access Rights
open access
CopyRight
This article is licensed under a Creative Commons Attribution 4.0 International License.
oaire:version
Version of Record
Category
学術雑誌論文 Journal Article