Fig. 4 Disruption of Kif17 splicing by an antisense morpholino oligonucleotide. (A) Mis-splicing of the Kif17 mRNA caused by blocking the exon 2 donor sequence. RT-PCR primers in exons 1 and 3 (small arrows) generate a smaller product in morphant embryos. (B) The morphant RT-PCR product sequence reveals an out of frame fusion to a cryptic splice donor within exon 2 resulting in a mRNA predicted to encode a Kif17 protein truncated at amino acid 102. (C) Morphant (mph) and control (invert sense) injected 3-day zebrafish larvae. (D) Western blots of 3-day embryos showing the reduction of Kif17 in morphants; anti-γ-tubulin was used as a loading control.
Reprinted from Developmental Biology, 316(1), Insinna, C., Pathak, N., Perkins, B., Drummond, I., and Besharse, J.C., The homodimeric kinesin, Kif17, is essential for vertebrate photoreceptor sensory outer segment development, 160-170, Copyright (2008) with permission from Elsevier. Full text @ Dev. Biol.