ArticlePLoS genetics2014
JNK controls the onset of mitosis in planarian stem cells and triggers apoptotic cell death required for regeneration and remodeling.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 112 citations in OpenAlex.
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- βcatenin-1 localization and transcriptomic profiling provide insights into the early development of planarians.BMC biology · 2025Article
- map3k1 suppresses terminal differentiation of migratory eye progenitors in planarian regeneration.PLoS genetics · 2025Article
- Cell Death Regulation by Smed-foxO in the Planarian Schmidtea mediterranea.Methods in molecular biology (Clifton, N.J.) · 2025Article
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- A PAK family kinase and the Hippo/Yorkie pathway modulate WNT signaling to functionally integrate body axes during regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Mechanistic regulation of planarian shape during growth and degrowth.Development (Cambridge, England) · 2024Article
- Biomarkers of chemotherapy-induced cardiotoxicity: toward precision prevention using extracellular vesicles.Frontiers in oncology · 2024Article
- MRLC controls apoptotic cell death and functions to regulate epidermal development during planarian regeneration and homeostasis.Cell proliferation · 2024Article
- Wnt/β-catenin signalling is required for pole-specific chromatin remodeling during planarian regeneration.Nature communications · 2023Article
- The role of the immune microenvironment in bone, cartilage, and soft tissue regeneration: from mechanism to therapeutic opportunity.Military Medical Research · 2022Review
- Injury-induced MAPK activation triggers body axis formation inProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Defined diets for freshwater planarians.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Strategies for Improving Photodynamic Therapy Through Pharmacological Modulation of the Immediate Early Stress Response.Methods in molecular biology (Clifton, N.J.) · 2022Review
- An Emerging Frontier in Intercellular Communication: Extracellular Vesicles in Regeneration.Frontiers in cell and developmental biology · 2022Review
- A MEKK1 - JNK mitogen activated kinase (MAPK) cascade module is active in Echinococcus multilocularis stem cells.PLoS neglected tropical diseases · 2021Article
- Decoding Stem Cells: An Overview on Planarian Stem Cell Heterogeneity and Lineage Progression.Biomolecules · 2021Review
- Apoptosis Quantification in Tissue: Development of a Semi-Automatic Protocol and Assessment of Critical Steps of Image Processing.Biomolecules · 2021Article
- Whole-Body Regeneration in the Lobate CtenophoreGenes · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regeneration of lost tissues depends on the precise interpretation of molecular signals that control and coordinate the onset of proliferation, cellular differentiation and cell death. However, the nature of those molecular signals and the mechanisms that integrate the cellular responses remain largely unknown. The planarian flatworm is a unique model in which regeneration and tissue renewal can be comprehensively studied in vivo. The presence of a population of adult pluripotent stem cells combined with the ability to decode signaling after wounding enable planarians to regenerate a complete, correctly proportioned animal within a few days after any kind of amputation, and to adapt their size to nutritional changes without compromising functionality. Here, we demonstrate that the stress-activated c-jun-NH2-kinase (JNK) links wound-induced apoptosis to the stem cell response during planarian regeneration. We show that JNK modulates the expression of wound-related genes, triggers apoptosis and attenuates the onset of mitosis in stem cells specifically after tissue loss. Furthermore, in pre-existing body regions, JNK activity is required to establish a positive balance between cell death and stem cell proliferation to enable tissue renewal, remodeling and the maintenance of proportionality. During homeostatic degrowth, JNK RNAi blocks apoptosis, resulting in impaired organ remodeling and rescaling. Our findings indicate that JNK-dependent apoptotic cell death is crucial to coordinate tissue renewal and remodeling required to regenerate and to maintain a correctly proportioned animal. Hence, JNK might act as a hub, translating wound signals into apoptotic cell death, controlled stem cell proliferation and differentiation, all of which are required to coordinate regeneration and tissue renewal.
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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.