Fig. 3

Reticulospinal ablation creates a target axon-deficient environment. a Stacked bar graph represents the proportion of myelin dedicated to transgene-labeled subtypes in the posterior spinal cord. n (larvae) = 10 (isl1[ss]⁺), 7 (tbx16⁺), 13 (Mauthner), 10 (phox2b⁺), 8 (pitx2c⁺). b Schematic depicting reticulospinal ablation. RB, C, and (RS) mark isl1[ss]⁺ RB cell bodies, tbx16⁺ CoPA cell bodies, and reticulospinal axons, respectively. Brackets enclose an area devoid of reticulospinal axons in ablated animals. c Lateral view images of the larval spinal cord acquired at 24 hpi (96 hpf) show severed, regenerating pitx2c⁺ axons alongside Wallerian degeneration of their former distal axon segments (left brackets). Arrowheads indicate growth cones of regenerating pitx2c⁺ axons, and brackets enclose areas devoid of reticulospinal axons. Note that severed axons never regenerated into posterior observation segments within 24 h of injury. Therefore, the posterior observation site lacked pitx2c⁺ descending reticulospinal axons, but possessed tbx16⁺ CoPA ascending local spinal interneurons. Images are tiled confocal maximum z-projections with dorsal up and anterior left. Scale bar = 20 μm