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. Author manuscript; available in PMC: 2015 Apr 1.
Published in final edited form as: Int J Dev Neurosci. 2013 Nov 23;33:41–48. doi: 10.1016/j.ijdevneu.2013.11.003

Figure 2. Identification of a defective cad allele as the gene responsible for the sl23 phenotype.

Figure 2

(A) Critical interval for the sl23 locus on chromosome 20, cad gene is in red. Arrows denote direction of transcription, numbers above map coordinates represent the number of recombinants out of 652 mutant larvae. (B) Alignment of the nucleotide sequences from exon 5 of the wild type and sl23 alleles: the missing 20 nucleotides are shown as dashes. The predicted frame shift encodes a novel amino acid sequence (shown in red) containing a stop codon. (C) Diagram of domains in the wildtype protein and the predicted null protein, showing the position of the deletion in sl23. (D) Rescue of the sl23 phenotype after injection of full-length wild-type Cad RNA into clutches of sl23+/− incrosses, supporting the mutant CAD gene as responsible for the sl23 phenotype. The data are shown as a bar graph (p≤0.1, one tail t-test). (E) Epifluorescent image of Tg(p2xr3.2:eGFP) injected with 250 µM Cad ATG morpholino. As seen in sl23 mutants, the central projections of the VII, IX and X sensory nerves are malformed.