ArticlePLoS genetics2014
Genetic models of apoptosis-induced proliferation decipher activation of JNK and identify a requirement of EGFR signaling for tissue regenerative responses in Drosophila.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 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
74 citing papers in PubMed, 115 citations in OpenAlex.
- Evasion of cell death despite mitochondrial outer membrane permeabilization: an oncogenic outcome of apoptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- The Hippo tumor suppressor pathway triggers non-cell autonomous tumorigenesis in Drosophila.EMBO reports · 2026Article
- Draper-mediated efferocytosis bybioRxiv : the preprint server for biology · 2026Article
- Single-cell RNA analysis reveals unexpected hemocyte plasticity and immune cell specialization in abioRxiv : the preprint server for biology · 2026Article
- Ythdc1-p300-Klf5 Complex-Mediated Golgi Dysfunction Promotes Aortic Aneurysm.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Calcium signaling regulates apoptosis-induced proliferation in Drosophila.PLoS biology · 2026Article
- Apoptosis-resistant cells drive compensatory proliferation via cell-autonomous and non-autonomous functions of the initiator caspase Dronc.Nature communications · 2025Article
- 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
- Cell Death, Compensatory Proliferation, and Cell Competition.Annual review of genetics · 2025Review
- Decoding the divide: what distinguishes apoptosis-induced proliferation from compensatory proliferation?Cell communication and signaling : CCS · 2025Review
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- Messages from Beyond the Grave: How Can Drosophila Help Us Understand the Consequences of Apoptosis?Advances in experimental medicine and biology · 2025Review
- Regeneration following tissue necrosis is mediated by non-apoptotic caspase activity.bioRxiv : the preprint server for biology · 2024Article
- Understanding the molecular mechanism of regeneration through apoptosis-induced compensatory proliferation studies - updates and future aspects.Apoptosis : an international journal on programmed cell death · 2024Review
- Intrinsic apoptosis is evolutionarily divergent among metazoans.Evolution letters · 2024Article
- Regenerative growth is constrained by brain tumor to ensure proper patterning in Drosophila.PLoS genetics · 2023Article
- Dissecting morphogenetic apoptosis through a genetic screen in Drosophila.Life science alliance · 2023Article
- Messenger functions of cell death during development and homeostasis.Biochemical Society transactions · 2023Article
- Physiological and molecular mechanisms of insect appendage regeneration.Cell regeneration (London, England) · 2023Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Recent work in several model organisms has revealed that apoptotic cells are able to stimulate neighboring surviving cells to undergo additional proliferation, a phenomenon termed apoptosis-induced proliferation. This process depends critically on apoptotic caspases such as Dronc, the Caspase-9 ortholog in Drosophila, and may have important implications for tumorigenesis. While it is known that Dronc can induce the activity of Jun N-terminal kinase (JNK) for apoptosis-induced proliferation, the mechanistic details of this activation are largely unknown. It is also controversial if JNK activity occurs in dying or in surviving cells. Signaling molecules of the Wnt and BMP families have been implicated in apoptosis-induced proliferation, but it is unclear if they are the only ones. To address these questions, we have developed an efficient assay for screening and identification of genes that regulate or mediate apoptosis-induced proliferation. We have identified a subset of genes acting upstream of JNK activity including Rho1. We also demonstrate that JNK activation occurs both in apoptotic cells as well as in neighboring surviving cells. In a genetic screen, we identified signaling by the EGFR pathway as important for apoptosis-induced proliferation acting downstream of JNK signaling. These data underscore the importance of genetic screening and promise an improved understanding of the mechanisms of apoptosis-induced proliferation.
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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.