Gcm counteracts Toll-induced inflammation and impacts hemocyte number through cholinergic signaling

Wael Bazzi , Sara Monticelli , Claude Delaporte (1) , Céline Riet (1) , Angela Giangrande (1) , Pierre Cattenoz (1)

1 IGBMC - Institut de Génétique et de Biologie Moléculaire et Cellulaire

Hemocytes, the myeloid-like immune cells of Drosophila, fulfill a variety of functions that are not completely understood, ranging from phagocytosis to transduction of inflammatory signals. We here show that downregulating the hemocyte-specific Glial cell deficient/Glial cell missing (Glide/Gcm) transcription factor enhances the inflammatory response to the constitutive activation of the Toll pathway. This correlates with lower levels of glutathione S-transferase, suggesting an implication of Glide/Gcm in reactive oxygen species (ROS) signaling and calling for a widespread anti-inflammatory potential of Glide/ Gcm. In addition, our data reveal the expression of acetylcholine receptors in hemocytes and that Toll activation affects their expressions, disclosing a novel aspect of the inflammatory response mediated by neurotransmitters. Finally, we provide evidence for acetylcholine receptor nicotinic acetylcholine receptor alpha 6 (nAchRalpha6) regulating hemocyte proliferation in a cell autonomous fashion and for non-cell autonomous cholinergic signaling regulating the number of hemocytes. Altogether, this study provides new insights on the molecular pathways involved in the inflammatory response.

Mots clés: hemocytes toll Glide/Gcm nAchRalpha6 inflammation Drosophila; hemocytes; toll; Glide/Gcm; nAchRalpha6; inflammation; Drosophila

Domaines: Sciences du Vivant [q-bio]

Wael Bazzi, Sara Monticelli, Claude Delaporte, Céline Riet, Angela Giangrande, et al.. Gcm counteracts Toll-induced inflammation and impacts hemocyte number through cholinergic signaling. Frontiers in Immunology, 2023, 14, ⟨10.3389/fimmu.2023.1293766⟩. ⟨hal-04295779⟩