Fig. 4
From: Dysregulation of innate immune signaling in animal models of spinal muscular atrophy
Targeted RNAi depletion of Smn in Drosophila immune cells yields melanotic masses and reduced viability. A Fraction of larvae that display MMs. RNAi-mediated knockdown of SMN was carried out using the Drosophila GAL4/UAS system to drive expression using two different RNAi transgenes, UAS-SmnJF (P|TRiP.JF02057|attP2) or UAS-SmnHM (P|TRiP.HMC03832|attP40). These lines were used together with the following GAL4- drivers: da, daughterless (da) for ubiquitous knockdown; C15 (a composite driver that includes elav- (embryonic lethal abnormal vision), sca- (scabrous) and BG57-GAL4 for knockdown in both neurons and muscles [53]; and Cg (Collagen 4a1 gap), for knockdown in the fat body, hemocytes, and the larval lymph gland [54]. OreR is the control strain. A plus sign ( +) indicates a wild-type chromosome. B Representative image of wild-type control and MMs in a larva with SMN depleted in the fat body, hemocytes, and lymph gland (Cg-Gal4 > UAS-SmnJF) or only in the hemocytes (Hml-Gal4 > UAS-SmnJF). C Number of MMs per animal with and without SMN depletion, as in A