Modeling of autosomal-dominant retinitis pigmentosa in Caenorhabditis elegans uncovers a nexus between global impaired functioning of certain splicing factors and cell type-specific apoptosis

(Downloading may take up to 30 seconds. If the slide opens in your browser, select File -> Save As to save it.)

Click on image to view larger version.

FIGURE 2.
FIGURE 2.

RNAi experiments classify s-adRP genes in two phenoclusters. (A) Developmental growth in animals treated with RNAi for s-adRP genes. Body length of wild-type worms with the indicated RNAi clones, starting from synchronized L1 and grown at 20°C. Mean body length of 50 worms per RNAi condition was scored at the indicated time points. Animal length was measured using the ImageJ software. Control worms were fed with the L4440 plasmid (empty vector). (B) Simplified scheme of the role of s-adRP genes in the splicing process. The six C. elegans s-adRP proteins are part of the tri-snRNP U4/U6·U5 complex. After the formation of the activated spliceosome, U5, but not U4, s-adRP proteins are required for subsequent splicing steps involving transesterification reactions. Exons are linked by thinner rectangles that represent an intron. White box: PRP-3, PRP-4, and PRP-31 are U4-specific, whereas PRP-6, PRP-8, and SNRNP-200 are U5-specific.

This Article

  1. RNA 21: 2119-2131