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Citation
Dimitriadou, A., Chatzianastasi, N., Zacharaki, P.I., O'Connor, M., Goldsmith, S.L., O'Connor, M.B., Consoulas, C., Newfeld, S.J. (2020). Adult Movement Defects Associated with a CORL Mutation in Drosophila Display Behavioral Plasticity.  G3 (Bethesda) 10(5): 1697--1706.
FlyBase ID
FBrf0245642
Publication Type
Research paper
Abstract

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 Fussel15 and Fussel18 with ataxia, we tested the hypothesis that dCORL mutations will cause adult movement disorders. For our initial tests, we conducted side by side studies of adults with the small deletion Df(4)dCORL and eight control strains. We found that deletion mutants exhibit three types of behavioral plasticity. First, significant climbing defects attributable to loss of dCORL are eliminated by age. Second, significant phototaxis defects due to loss of dCORL are partially ameliorated by age and are not due to faulty photoreceptors. Third, Df(4)dCORL males raised in groups have a lower courtship index than males raised as singles though this defect is not due to loss of dCORL Subsequent tests showed that the climbing and phototaxis defects were phenocpied by dCORL21B and dCORL23C two CRISPR generated mutations. Overall, the finding that adult movement defects due to loss of dCORL are subject to age-dependent plasticity suggests new hypotheses for CORL functions in flies and mammals.

PubMed ID
PubMed Central ID
PMC7202012 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    G3 (Bethesda)
    Title
    G3 : genes - genomes - genetics
    ISBN/ISSN
    2160-1836
    Data From Reference
    Aberrations (1)
    Alleles (7)
    Genes (4)
    Insertions (3)