Synergistic interaction of hKir2.1 and PlexinA3. Percentage of (A) RoPs extending their axons rostrally or bypassing the endogenous exit point or (B) MiP axons with aberrant branching, including data from Fig. 6. Combination of a subthreshold concentration of PlexinA3 MO and hKir2.1 expression generates an increase in the incidence of pathfinding errors. Control, embryos injected with Hb9:Gal4 and UAS:DsRed plasmids; Kir, embryos injected with Hb9:Gal4 and UAS:DsRed::UAS:hKir2.1 plasmids; MO 0.5 mM, embryos injected with 0.5 mM PlexinA3 MO and Hb9:Gal4 and UAS:DsRed plasmids; MO 0.3 mM, embryos injected with 0.3 mM PlexinA3 MO and Hb9:Gal4 and UAS:DsRed plasmids; MO 0.3 mM + Kir, embryos injected with 0.3 mM PlexinA3 MO and Hb9:Gal4 and UAS:DsRed::UAS:hKir2.1 plasmids; 5 mm MO + Kir, embryos injected with 0.3 mM MO with five mismatched bases based on PlexinA3 MO and Hb9:Gal4 and UAS:DsRed::UAS:hKir2.1 plasmids. n = 30–40 neurons from e30 24-hpf embryos for each condition. *P < 0.05 using a Fisher exact test comparing PlexinA3 MO + Kir-injected with Kir-injected alone. (C–E) Single PMN expressing hKir2.1 and DsRed and exhibiting a pathfinding error expresses PlexinA3 mRNA. (C) A DsRed immunopositive RoP extending its axon rostrally. (D) In situ hybridization shows strong expression of PlexinA3 mRNA. (E) Merge of C and D. Dorsal is to the top and rostral is to the left. Dot-dash lines mark lateral edges of the myotomes; dotted lines mark the ventral edge of the spinal cord. n = 4 MiPs, and n = 4 RoPs.
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