Fig. S2

PGRN rescues motor axon defects produced by TDP-43 or FUS knockdown in WT embryos.

S2A Top panel. PGRN rescues motor axon defects produced by TDP-43 Knockdown in WT embryos. TDP-43 knockdown produced shorter axons that were rescued by co-injection of hPGRN mRNA. Lateral views (anterior to the left; dorsal to the top) of embryos labelled with znp1 mAb at 27 hpf in wild-type embryos, embryos injected with TDP-43 AMO, embryos co-injected with hPGRN mRNA (TDP-43AMO+hPGRN). Embryos co-injected with hPGRN mRNA (TDP-43AMO+hPGRN) partially reversed the truncation phenotype. Observed phenotypes were normal MN development (WT), increase in truncated and branched axons (TDP43 MO) and partial rescue of truncated MNs (TDP43 MO+PGRN). Dashed lines represent the horizontal myoseptum. S2A Fig bottom panel. PGRN rescues motor axon defects induced by FUS knockdown. FUS knockdown produced shorter axons that were rescued by hPGRN mRNA. Lateral views (anterior to the left; dorsal to the top) of embryos labelled with znp1 mAb at 27 hpf in wild type embryos, embryos injected with FUS AMO, embryos co-injected with hPGRN mRNA (FUS AMO +hPGRN). Embryos co-injected with hPGRN mRNA (FUS AMO+hPGRN) partially reversed truncation phenotype. Observed phenotypes were normal MN development (WT), increase in truncated and branched axons (FUS MO) and partial rescue of truncated MNs (FUS MO+PGRN). Dashed lines represent horizontal myoseptum. Images were captured at 20X magnification and the hatched box was further subject to 4-5X Zoom. S2B Fig TDP-43 knockdown and partial rescue with over-expression of PGRN mRNA in WT embryos. Average number of Truncated (B1) and Branched (B2) CaP MNs per group. S2C Fig. FUS knockdown and partial rescue with over-expression of PGRN. Average number of Branched (C1) and Truncated (C2) CaP MNs per group.