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Heins-Marroquin et al., 2025 - Pex1 loss-of-function in zebrafish is viable and recapitulates hallmarks of Zellweger spectrum disorders

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FIGURE 1

Generation of a pex1 zebrafish model by CRISPR/Cas9. (A,B) Targeting CRISPR sites in exon 5 of the zebrafish pex1 gene induced a 17 bp-deletion leading to a premature stop codon (MUT). (C) PCR on genomic DNA allows genotyping: wild-type (WT, 290 bp), heterozygous, and homozygous mutant (273 bp). (D) Amino-acid sequences of wildtype (WT, 1273 aa) versus mutated Pex1 protein (MUT, 305 aa), which is predicted to lack the AAA-ATPase domains essential for Pex1 function. The altered amino acid sequence resulting from the frameshift mutation is indicated in orange. (E) Proteomics-based analysis of Pex protein levels in livers from 7-month-old WT and pex1^–/– zebrafish (data are means ± % CV for n = 3 biological replicates).

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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 @ Front. Mol. Neurosci.