Cytokine/Jak/Stat signaling mediates regeneration and homeostasis in the Drosophila midgut
By Huaqi Jiang, Parthive H. Patel, Alexander Kohlmaier, M. Grenley, D. McEwen, Bruce Edgar. Cell, 2009
1,020 citations recorded by the source corpus.
SUMMARY Cells in intestinal epithelia turn over rapidly due to damage from digestion and toxins produced by the enteric microbiota. Gut homeostasis is maintained by intestinal stem cells (ISCs) that divide to replenish the intestinal epithelium, but little is known about how ISC division and differentiation are coordinated with epithelial cell loss. We show here that when enterocytes (ECs) in the Drosophila midgut are subjected to apoptosis, enteric infection, or JNK-mediated stress signaling, they produce cytokines (Upd, Upd2, Upd3) that activate Jak/Stat signaling in ISCs, promoting their rapid division. Upd/Jak/Stat activity also promotes progenitor cell differentiation, in part by stimulating Delta/Notch signaling, and is required for differentiation in both normal and regenerating midguts. Hence, cytokine-mediated feedback enables stem cells to replace spent progeny as they are lost, thereby establishing gut homeostasis.
Subfields: Immunology, Insect Science
View Paper: https://www.semanticscholar.org/paper/c4bffbdefda7b3d734ee84622ab4288858dc8eff
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Citations in the corpus
- Invasive and indigenous microbiota impact intestinal stem cell activity through multiple pathways in Drosophila. (2009, background): “In contrast to the requirement of the JNK pathway upon Ecc15 infection, Jiang et al. (2009) reported that oral ingestion with a low dose of P. entomophila still induced mitosis in the JNK-defective mutant hep1.”
- The gut microbiota of insects - diversity in structure and function. (2013, background): “Bacteria in the midgut modulate this stem cell activity, probably by inducing epithelial cell damage and apoptosis, which results in the activation the JAK-STAT signaling pathway (Buchon et al., 2009b; Cronin et al., 2009; Jiang et al., 2009).”