Genetic interactors were found to cause lamina plexus defects with Dys and Dg. (A) Wild type properly formed lamina plexus and defects found in Dg (and Dys) mutants showing gaps in the axon projections (arrows). 24B10 antibody was used to visualize photoreceptor axons. (B) Dys and Dg homozygous mutants have a significantly higher percentage of these defects from control and genetically interact. (C) Genetic interactions found with Dys, and with Dg (D). Statistics were determined using the χ2-test with Yate's correction where ***p ≤ 0.001, **p ≤ 0.01, *p ≤ 0.05.
Marrone et al. BMC Neuroscience 2011 12:93 doi:10.1186/1471-2202-12-93