Adult Movement Defects Associated with a CORL Mutation in Display Behavioral Plasticity.

The CORL family of CNS-specific proteins share a Smad-binding region with mammalian SnoN and c-Ski protooncogenes. In this family Drosophila CORL has two mouse and two human relatives. Roles for the mouse and human CORL proteins are largely unknown. Based on genome-wide association studies linking the human CORL proteins and with ataxia, we tested the hypothesis that mutations will cause adult movement disorders. For our initial tests, we conducted side by side studies of adults with the small deletion and eight control strains. We found that deletion mutants exhibit three types of behavioral plasticity. First, significant climbing defects attributable to loss of are eliminated by age. Second, significant phototaxis defects due to loss of are partially ameliorated by age and are not due to faulty photoreceptors. Third, males raised in groups have a lower courtship index than males raised as singles though this defect is not due to loss of Subsequent tests showed that the climbing and phototaxis defects were phenocpied by and two CRISPR generated mutations. Overall, the finding that adult movement defects due to loss of are subject to age-dependent plasticity suggests new hypotheses for CORL functions in flies and mammals.