ArticlePLoS genetics2022
Actin remodeling mediates ROS production and JNK activation to drive apoptosis-induced proliferation.
Article in PLoS genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Experimental and molecular docking evidence for the protective role of Monascus purpureus red pigments against hydroxyapatite nanoparticle-induced testicular injury in male rats.Scientific reports · 2026Article
- Nicotinamide adenine dinucleotide phosphate oxidase 4 in lung disease: a review of its biology and therapeutic potential.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- 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
- Functional Division of Insect Blood Cells by Single-Cell RNA-Sequencing and Cell-Type-Specific FISH Markers.Cells · 2025Article
- Cell Death, Compensatory Proliferation, and Cell Competition.Annual review of genetics · 2025Review
- Neuronal branching in stem cell models of mitochondrial and neurological diseases.Stem cells (Dayton, Ohio) · 2025Review
- Regulation of host immunity by a novel Legionella pneumophila E3 ubiquitin ligase.PLoS pathogens · 2025Article
- Targeting Cancer Cell Fate: Apoptosis, Autophagy, and Gold Nanoparticles in Treatment Strategies.Current issues in molecular biology · 2025Review
- Apoptotic mesenchymal stem cells and their secreted apoptotic extracellular vesicles: therapeutic applications and mechanisms.Stem cell research & therapy · 2025Review
- Saikosaponin A Mediates the Anti-Acute Myeloid Leukemia Effect via the P-JNK Signaling Pathway Induced by Endoplasmic Reticulum Stress.Drug design, development and therapy · 2025Article
- The role of the PKCζ/JNK signaling pathway in regulating the development of femoral head necrosis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025Article
- A comprehensive analysis of the defense responses of Odontotermes formosanus (Shiraki) provides insights into the changes during Serratia marcescens infection.BMC genomics · 2024Article
- Reactive oxygen species activate the Drosophila TNF receptor Wengen for damage-induced regeneration.The EMBO journal · 2024Article
- Riding the Wave of Ambivalence in Cell Biology.International journal of molecular sciences · 2024Article
- The JNK signaling pathway in intervertebral disc degeneration.Frontiers in cell and developmental biology · 2024Review
- Messenger functions of cell death during development and homeostasis.Biochemical Society transactions · 2023Article
- Growth hormone-releasing hormone antagonists counteract hydrogen peroxide - induced paracellular hyperpermeability in endothelial cells.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research SocietyArticle
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Stress-induced cell death, mainly apoptosis, and its subsequent tissue repair is interlinked although our knowledge of this connection is still very limited. An intriguing finding is apoptosis-induced proliferation (AiP), an evolutionary conserved mechanism employed by apoptotic cells to trigger compensatory proliferation of their neighboring cells. Studies using Drosophila as a model organism have revealed that apoptotic caspases and c-Jun N-terminal kinase (JNK) signaling play critical roles to activate AiP. For example, the initiator caspase Dronc, the caspase-9 ortholog in Drosophila, promotes activation of JNK leading to release of mitogenic signals and AiP. Recent studies further revealed that Dronc relocates to the cell cortex via Myo1D, an unconventional myosin, and stimulates production of reactive oxygen species (ROS) to trigger AiP. During this process, ROS can attract hemocytes, the Drosophila macrophages, which further amplify JNK signaling cell non-autonomously. However, the intrinsic components connecting Dronc, ROS and JNK within the stressed signal-producing cells remain elusive. Here, we identified LIM domain kinase 1 (LIMK1), a kinase promoting cellular F-actin polymerization, as a novel regulator of AiP. F-actin accumulates in a Dronc-dependent manner in response to apoptotic stress. Suppression of F-actin polymerization in stressed cells by knocking down LIMK1 or expressing Cofilin, an inhibitor of F-actin elongation, blocks ROS production and JNK activation, hence AiP. Furthermore, Dronc and LIMK1 genetically interact. Co-expression of Dronc and LIMK1 drives F-actin accumulation, ROS production and JNK activation. Interestingly, these synergistic effects between Dronc and LIMK1 depend on Myo1D. Therefore, F-actin remodeling plays an important role mediating caspase-driven ROS production and JNK activation in the process of AiP.
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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.