Fig. 1. lyr is a new allele of the Ncad mutant, pac. (A,B) Lateral views of 3 dpf wild-type (A) and lyr^–/– (B) eyes labeled with anti-acetylated -tubulin antibody. Arrowheads indicate disruption of the IPL. (C) Map of microsatellite markers used to map lyr to the same position on LG20 as ncad. Recombination rate is indicated by parenthesis. (D,E) Lateral views of wild-type (D) and mutant (E) embryos produced by crossing lyr and pac^fr7 carriers. Morphological defects are evident in the tectum and hindbrain of the mutant (E, arrowheads). (F) Mutation sites in the two pac alleles used in this study. A nonsense mutation present in pac ^fr7 (Lele et al., 2002) and a mis-sense mutation (TyrCys) found in lyr^–/– embryos both occur in EC4 domain of Ncad. (G,H) Confocal images of aggregates of cells in which animal caps labeled with Alexa-488 conjugated dextran (green) and expressing either wild-type Ncad RNA (G) or lyr-mutated Ncad RNA (H) were juxtaposed to non-injected animal caps labeled with rhodamine-conjugated dextran (red). The sharp boundary between the Ncad-expressing and non-expressing cell masses is disrupted by the lyr mutation. (I) Quantification of cell intermingling. The bars indicate the average number of cells isolated within the apposing animal cap. Numbers of animal caps examined are indicated under the columns. h, hindbrain; inl, inner nuclear layer; ipl, inner plexiform layer; MHB, midbrain-hindbrain boundary; onl, outer nuclear layer; rgl, retinal ganglion cell layer; Tc, optic tectum.

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