Fig. S1

In larval zebrafish, mutations in gdf6a do not appreciably sensitize SOD1ΛG93R zebrafish to develop ALS-like symptoms. Four genotypes combining Gdf6^-/- alleles and SOD1ΛG93R alleles were examined in Tg(HB9:eGFP) zebrafish expressing GFP in the axons of primary motor neurons (PMN), or via immunohistochemistry. A. Bracket indicates position of axons quantified, magnified in B,C. B. Normal primary motor axons. C. An example of an abnormal PMN axon (arrow). D. Quantification of primary motor axons in 30 hour post-fertilization embryosshow no difference based on gdf6a genotype; Thus effects are not developmental, and accord with a late-onset phenotype. Results indicated no significant effect of Gdf6 on the presence of axonopathies (p≥0.315, n≥5 larvae per genotype), although the highest rate of PMN axon abnormalities were observed in gdf6a^-/-;SOD1^+/G93R larvae.