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Fig. 6 Transient knockdown of parkin in zebrafish does not lead to gross morphological alterations.
(A) Genomic structure of zebrafish parkin comprising a total of 12 exons. The splice-blocking GT-grip targets the exon-intron junction of exon 2. (B+C) Verification of the parkin knockdown efficiency by semi-quantitative real-time PCR. (B) The TaqMan™ probe targets the exon 2/exon 3 junction and cannot bind in case of incorrect splicing. (C) Parkin knockdown efficiency at day 1, 2 and 3 after injection of the parkin-specific GT-grip in comparison to a control GT-grip. The amount of zebrafish parkin-specific mRNA was normalized to β-actin in parkin GT-grip-injected zebrafish compared to control GT-grip-injected zebrafish. Quantification is based on 4 independent experiments. ***p<0.001 (D) Parkin-deficient zebrafish embryos do not show obvious morphological alterations. Two-day-old parkin knockdown zebrafish embryos are shown in comparison to control-injected embryos.