Fig. 2.

DRK is recruited to glial membranes surrounding the injured axons. (A) Endogenous DRK (red, α-DRK) in glia was recruited to the severed mp nerves labeled with OR85e-mCD8::GFP (green, α-GFP) 1 d after axotomy. Before injury, DRK expression was evenly distributed in the SOG but not colocalized with the OR85e⁺ maxillary nerve. One day after mp injury, DRK expression was increased around the degenerating maxillary nerves (arrowheads), which was not seen in drk^RNAi animals. Representative images (single slice) are shown. (Scale bar: 10 μm.) (B) Endogenous DRK expression in glia was increased 1 d after axotomy. Glial membranes were labeled with mCD8::GFP by glia-specific repo-Gal4 driver. Antennal ablation (removal of the third segment of antennae) was performed to induce a greater extent of axon degeneration in the antennal lobe (AL). Normally, thin glial membranes ensheath (arrows) the antennal lobe and each glomerulus (no injury, control). However, 1 d after antennal ablation, ensheathing glia became hypertrophy (1 d after injury, dashed lines), and strong DRK immunoreactivity (red) was found in hypertrophic region of ensheathing glia (yellow), but not when drk^RNAi was expressed by repo-Gal4, indicating that the increase of DRK is glia-specific. Representative images (single slice) are shown. C, cortex. (Scale bar: 10 μm.)