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. 2020 Apr 22;40(17):3360–3373. doi: 10.1523/JNEUROSCI.1397-19.2020

Figure 3.

Figure 3.

Perineurial glia-specific knockdown of Bsg causes VNC shortening, peripheral glial abnormalities, and reduced larval locomotion. A, B, The VNC of third instar Drosophila larvae expressing endogenously tagged Bsg::GFP (green) and 46F-GAL4 driving expression of mCD8::RFP (magenta). Knockdown of Bsg in the perineurial glia using Bsg-RNAi results in shortening of the VNC (B) compared with controls (A) and a loss of Bsg expression in the glia ensheathing the CNS and PNS while expression is retained in the neuropil (asterisks) and the NMJs (arrowheads). Scale bar, 50 μm. C-F, Peripheral nerve of third instar 46F>mCD8::RFP (green) larvae with axons labeled using anti-Futsch/22C10 (magenta). Bsg knockdown results in compression of the glia (D, asterisk), and knockdown in a heterozygous Bsg mutant (Bsg[265]) exacerbates the phenotype (F, asterisk). Scale bars, 15 μm. G, Bsg knockdown results in significant shortening of the VNC (****p < 0.0001) compared with control (46F-GAL4). H, Penetrance of glial compression was significantly increased in the background heterozygous for Bsg[265] (*p = 0.0088) compared with control (46F-GAL4) and Bsg-RNAi alone. I, Knockdown of Bsg (magenta) and the integrin β-subunit myospheroid (mys) (orange) significantly reduced larval locomotion (****p < 0.001) compared with control 46F>Dicer2 (green). *p < 0.05, ****p < 0.0001.