Figure 1.

Modeling the Noonan syndrome‐associated loss‐of‐function LZTR1 mutations in zebrafish. (a) CRISPR/Cas9‐based gene targeting induced a 7‐bp frameshift deletion in exon 2 of the zebrafish (Danio rerio) lztr1. (b) Quantitative PCR analysis of the lztr1 transcript showed comparable expression levels between different genotypes. Data are represented as the mean ± SD of technical triplicates from a representative experiment. (c) The effect of CRISPR induced 7‐bp frameshift deletion on lztr1 mRNA and protein sequence. (d) GST‐tagged wild‐type and mutated proteins were detected by western blot using anti‐GST antibody. The 7‐bp frameshift deletion resulted in premature truncation of the LZTR1 protein