FIGURE

Fig. 1

ID

ZDB-FIG-250410-14

Publication

Liu et al., 2025 - Knockout of the fcsk gene in zebrafish causes neurodevelopmental defects

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Fig. 1

CRISPR/Cas9-mediated fcsk knockout in zebrafish A: CRISPR/Cas9 target sites in fcsk. B: Sanger sequencing confirmed a five-base deletion (c.160_164delTGGGA, p.W54Rfs*13) in F2 generation of fcsk−/− zebrafish. C: fcsk mutation abolished the NcoI cleavage site, preventing digestion of the PCR products in homozygous (fcsk−/−) zebrafish (372 bp). In contrast, PCR products from WT zebrafish were cleaved into 190 bp and 187 bp fragments, while heterozygous (fcsk+/−) zebrafish exhibited digestion of the WT allele, resulting in 372 bp, 190 bp, and 187 bp fragments. D: Protein structure of human FCSK (h FCSK), zebrafish WT Fcsk (zf Fcsk) and mutant Fcsk (zf Fcsk−/−). E: Relative mRNA levels of fcsk in fcsk−/− zebrafish (5 dpf) were detected by semi-quantitative RT-PCR. dpf: Days post-fertilization. Results are presented as mean±SEM, n=3. **: P<0.01.

Expression Data

Gene:	fcsk
Fish:	AB fcsk^{hzu301/hzu301} (AB)
Anatomical Term:	whole organism
Stage:	Day 5

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	fcsk^{hzu301/hzu301} (AB)
Observed In:	whole organism
Stage:	Day 5

Phenotype Detail

Acknowledgments

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