ArticleCell death and differentiation2012
A dp53/JNK-dependant feedback amplification loop is essential for the apoptotic response to stress in Drosophila.
Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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94 citing papers in PubMed, 141 citations in OpenAlex.
- Short-term memory of past caspase activity biases cell elimination in vivo.Nature communications · 2026Article
- The signaling and regulatory functions of dying cells and cell corpses.Communications biology · 2026Review
- Transcription-dependent and -independent functions of Drosophila p53 isoforms in the induction of apoptosis and senescence-associated tumorigenesis.Cell death & disease · 2026Article
- Single-cell transcriptomics of X-ray irradiatedeLife · 2026Article
- The homeodomain-interacting protein kinase Hipk promotes apoptosis by stabilizing the active form of Dronc.Cell death discovery · 2025Article
- 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
- Article
- Replication stress promotes cellular transformation in Drosophila epithelium.Cell death discovery · 2025Article
- Messages from Beyond the Grave: How Can Drosophila Help Us Understand the Consequences of Apoptosis?Advances in experimental medicine and biology · 2025Review
- Reactive oxygen species activate the Drosophila TNF receptor Wengen for damage-induced regeneration.The EMBO journal · 2024Article
- Unraveling the Immune Regulatory Functions of USP5: Implications for Disease Therapy.Biomolecules · 2024Review
- A feedback loop that drives cell death and proliferation and its defect in intestinal stem cells.Life science alliance · 2024Article
- A conserved mechanism for JNK-mediated loss of Notch function in advanced prostate cancer.Science signaling · 2023Article
- Hijacking homeostasis: Regulation of the tumor microenvironment by apoptosis.Immunological reviews · 2023Review
- Nacα protects the larval fat body from cell death by maintaining cellular proteostasis in Drosophila.Nature communications · 2023Article
- Lack of apoptosis leads to cellular senescence and tumorigenesis in Drosophila epithelial cells.Cell death discovery · 2023Article
- Mutual repression between JNK/AP-1 and JAK/STAT stratifies senescent and proliferative cell behaviors during tissue regeneration.PLoS biology · 2023Article
- Messenger functions of cell death during development and homeostasis.Biochemical Society transactions · 2023Article
34 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Programmed cell death (apoptosis) is a conserved process aimed to eliminate unwanted cells. The key molecules are a group of proteases called caspases that cleave vital proteins, which leads to the death of cells. In Drosophila, the apoptotic pathway is usually represented as a cascade of events in which an initial stimulus activates one or more of the proapoptotic genes (hid, rpr, grim), which in turn activate caspases. In stress-induced apoptosis, the dp53 (Drosophila p53) gene and the Jun N-terminal kinase (JNK) pathway function upstream in the activation of the proapoptotic genes. Here we demonstrate that dp53 and JNK also function downstream of proapoptotic genes and the initiator caspase Dronc (Drosophila NEDD2-like caspase) and that they establish a feedback loop that amplifies the initial apoptotic stimulus. This loop plays a critical role in the apoptotic response because in its absence there is a dramatic decrease in the amount of cell death after a pulse of the proapoptotic proteins Hid and Rpr. Thus, our results indicate that stress-induced apoptosis in Drosophila is dependant on an amplification loop mediated by dp53 and JNK. Furthermore, they also demonstrate a mechanism of mutual activation of proapoptotic genes.
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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.