Fig. 3
- ID
- ZDB-FIG-130625-41
- Publication
- Schmid et al., 2013 - Loss of ALS-associated TDP-43 in zebrafish causes muscle degeneration, vascular dysfunction, and reduced motor neuron axon outgrowth
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tardbp-/-;tardbpl-/- mutants have impaired blood circulation that can be rescued. (A) tardbp-/-;tardbpl-/- mutants accumulate erythrocytes on the yolk (arrow) because of a lack of circulation at 2 dpf. Anterior to the left. See also Movie S1. (B) The circulation phenotype can be restored by injection of mRNA encoding human TDP-43 and zebrafish Tardbpl_tv1, but not by the shorter isoform Tardbpl. Injection of mRNA of the ALS-associated TDP-43G348C also rescues the circulation phenotype, whereas mRNA of the ALS-associated gene FUS fails to rescue. The black bar represents uninjected double homozygous mutant siblings of each respective clutch. The expected 25% of double-homozygous mutant embryos from incrosses of tardbp-/-;tardbpl+/- or tardbp+/-;tardbpl-/- fish were set to 100%. Error bars indicate ±SD, n e 182 embryos per experiment. *, P < 0.05; ***, P < 0.005, student t test. |