ArticleCell reports2024
Transient caspase-mediated activation of caspase-activated DNase causes DNA damage required for phagocytic macrophage differentiation.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed.
- Evasion of cell death despite mitochondrial outer membrane permeabilization: an oncogenic outcome of apoptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- COP9 signalosome regulates EGFR and Notch signaling during myeloid-type progenitor cell fate decision in Drosophila.EMBO reports · 2026Article
- Clinical application of liquid biopsy in the diagnosis and treatment of lung cancer: taking ctDNA for example-a narrative review.Journal of thoracic disease · 2026Review
- Porcine reproductive and respiratory syndrome virus N protein-mediated viral replication enhancement via interaction with host caspase-6.Journal of virology · 2026Article
- What does BCL-2 do? From new molecular insights to the clinical implications.Cell death and differentiation · 2026Review
- Caspase-Activated DNase localizes to cancer causing translocation breakpoints during cell differentiation.bioRxiv : the preprint server for biology · 2024Article
- Dual role for Headcase in hemocyte progenitor fate determination in Drosophila melanogaster.PLoS genetics · 2024Article
- Larval hematopoietic organs of multiplemicroPublication biology · 2024Article
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Abstract
Phagocytic macrophages are crucial for innate immunity and tissue homeostasis. Most tissue-resident macrophages develop from embryonic precursors that populate every organ before birth to lifelong self-renew. However, the mechanisms for versatile macrophage differentiation remain unknown. Here, we use in vivo genetic and cell biological analysis of the Drosophila larval hematopoietic organ, the lymph gland that produces macrophages. We show that the developmentally regulated transient activation of caspase-activated DNase (CAD)-mediated DNA strand breaks in intermediate progenitors is essential for macrophage differentiation. Insulin receptor-mediated PI3K/Akt signaling regulates the apoptosis signal-regulating kinase 1 (Ask1)/c-Jun kinase (JNK) axis to control sublethal levels of caspase activation, causing DNA strand breaks during macrophage development. Furthermore, caspase activity is also required for embryonic-origin macrophage development and efficient phagocytosis. Our study provides insights into developmental signaling and CAD-mediated DNA strand breaks associated with multifunctional and heterogeneous macrophage differentiation.
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