Fig. 5

Innate immune signaling pathways contribute to MMs upon SMN depletion. A Diagram summarizing the features and interconnections between innate immune signaling pathways in Drosophila. Bendless/Ubc13 (Ben) is an E2 ubiquitin conjugase that heterodimerizes with Uev1a and functions in a complex (boxed in gray) with Effete/Ubc5 (another E2) and two different E3 ligases (Traf6 for TLR/Toll or TNF/Wgn, and Diap2 for the Imd/PGRP pathway). The Immune Deficiency protein (Imd) serves not only as a receptor-proximal signaling factor, but also as a secondary substrate for K63-linked polyubiquitylation via Ben•Uev1a. Bendless thus sits at a node that connects many different signaling pathways and cellular processes. B Mutations in the IMD and Toll signaling pathways suppress the number of MMs per animal in Smn RNAi lines. Reduced dosage of Protein Arginine Methyltransferase 5 (PRMT5) also suppresses MMs upon depletion of SMN. C MMs per animal were measured following co-expression of an Smn RNAi transgene together with the indicated RNAi lines targeting selected members of the Toll and IMD pathways, as well as to genes encoding the Jumonji domain containing 6 (JMJD6), Gemin 2 (Gem2), and refractory to sigma P (ref(2)P) proteins. Co-expression of UAS:NLS-GFP was used as a Gal4 negative control (see text for details). D Pie chart of the identified enhancers and suppressors of MM formation, resulting from Smn RNAi depletion using the Cg-Gal4 driver. See Table 1 for details.