ArticleDevelopmental cell2014
Multiple mechanisms modulate distinct cellular susceptibilities toward apoptosis in the developing Drosophila eye.
Article in Developmental cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
- Calcium signaling regulates apoptosis-induced proliferation in Drosophila.PLoS biology · 2026Article
- Distinct roles of clustered MicroRNAs miR-286 and miR-6 in JNK activation critical to apoptosis-induced proliferation in Drosophila.Cellular and molecular life sciences : CMLS · 2025Article
- Critical roles ofLife science alliance · 2025Article
- Tolerance thresholds underlie responses to DNA damage during germline development.Genes & development · 2024Article
- Deciphering the link: ferroptosis and its role in glioma.Frontiers in immunology · 2024Review
- The histone demethylase Kdm5 controls Hid-induced cell death inFrontiers in cell death · 2024Article
- Actin remodeling mediates ROS production and JNK activation to drive apoptosis-induced proliferation.PLoS genetics · 2022Article
- Ferroptosis and Its Potential Role in Glioma: From Molecular Mechanisms to Therapeutic Opportunities.Antioxidants (Basel, Switzerland) · 2022Review
- An Open Question: Is Non-Ionizing Radiation a Tool for Controlling Apoptosis-Induced Proliferation?International journal of molecular sciences · 2021Review
- The Hh pathway promotes cell apoptosis through Ci-Rdx-Diap1 axis.Cell death discovery · 2021Article
- E3 ubiquitin ligase-mediated regulation of vertebrate ocular development; new insights into the function of SIAH enzymes.Biochemical Society transactions · 2021Review
- Characterization of TNF-induced cell death in Drosophila reveals caspase- and JNK-dependent necrosis and its role in tumor suppression.Cell death & disease · 2019Article
- Fate mapping during regeneration: Cells that undergo compensatory proliferation in damaged Drosophila eye imaginal discs differentiate into multiple retinal accessory cell types.Developmental biology · 2018Article
- Fizzy-Related dictates A cell cycle switch during organ repair and tissue growth responses in theeLife · 2018Article
- An unexpected friend - ROS in apoptosis-induced compensatory proliferation: Implications for regeneration and cancer.Seminars in cell & developmental biology · 2018Review
- Plasma Membrane Localization of Apoptotic Caspases for Non-apoptotic Functions.Developmental cell · 2018Article
- Atf3 links loss of epithelial polarity to defects in cell differentiation and cytoarchitecture.PLoS genetics · 2018Article
- Article
- Killers creating new life: caspases drive apoptosis-induced proliferation in tissue repair and disease.Cell death and differentiation · 2017Review
- Transitional Progenitors during Vertebrate Retinogenesis.Molecular neurobiology · 2017Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Although apoptosis is mechanistically well understood, a comprehensive understanding of how cells modulate their susceptibility toward apoptosis in a developing tissue is lacking. Here, we reveal striking dynamics in the apoptotic susceptibilities of different cell types in the Drosophila retina over a period of only 24 hr. Mitotic cells are extremely susceptible to apoptotic signals, while postmitotic cells have developed several strategies to promote survival. For example, photoreceptor neurons accumulate the inhibitor of apoptosis, Diap1. In unspecified cells, Cullin-3-mediated degradation keeps Diap1 levels low. These cells depend on EGFR signaling for survival. As development proceeds, developmentally older photoreceptors degrade Diap1, resulting in increased apoptosis susceptibility. Finally, R8 photoreceptors have very efficient survival mechanisms independent of EGFR or Diap1. These examples illustrate how complex cellular susceptibility toward apoptosis is regulated in a developing organ. Similar complexities may regulate apoptosis susceptibilities in mammalian development, and tumor cells may take advantage of it.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.