Fig. 4
- ID
- ZDB-FIG-080411-21
- Publication
- Insinna et al., 2008 - The homodimeric kinesin, Kif17, is essential for vertebrate photoreceptor sensory outer segment development
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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. |
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Stage: | Protruding-mouth |
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.