FIGURE

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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Fig. 3

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-43^G348C 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.

Expression Data

Expression Detail

Antibody Labeling

Phenotype Data

Phenotype Detail

Acknowledgments

This image is the copyrighted work of the attributed author or publisher, and ZFIN has permission only to display this image to its users. Additional permissions should be obtained from the applicable author or publisher of the image. Full text @ Proc. Natl. Acad. Sci. USA