FIGURE

FIGURE 4

ID

ZDB-FIG-210708-89

Publication

Uehara et al., 2021 - Recurrent NFIA K125E substitution represents a loss-of-function allele: Sensitive in vitro and in vivo assays for nontruncating alleles

Other Figures

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FIGURE 4

Commissural defects in nfia mutant zebrafish. Commissural axons (arrows) cross the midline in the midbrain/hindbrain boundary in wild‐type (a) (n = 4/4) and nfia heterozygous mutant (b) (n = 6/6) embryos at 3 dpf, but many of them failed to do so in nfia homozygous mutants (c) (n = 5/5). The midline crossing defects in nfia homozygous mutants were rescued by injection of NFIA^WT mRNA (d) (n = 5/5), but not by that of NFIA^K125E one (e) (n = 5/5). Axons were labeled with anti‐acetylated α‐tubulin antibody [Color figure can be viewed at wileyonlinelibrary.com]

Expression Data

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	nfia^{sa16768/sa16768}
Observed In:	caudal commissure axon central nervous system development hindbrain commissure axon
Stage:	Protruding-mouth

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 @ Am. J. Med. Genet. A