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ABSTRACT: Background
Although habituation is one of the most ancient and fundamental forms of learning, its regulators and its relevance for human disease are poorly understood.Methods
We manipulated the orthologs of 286 genes implicated in intellectual disability (ID) with or without comorbid autism spectrum disorder (ASD) specifically in Drosophila neurons, and we tested these models in light-off jump habituation. We dissected neuronal substrates underlying the identified habituation deficits and integrated genotype-phenotype annotations, gene ontologies, and interaction networks to determine the clinical features and molecular processes that are associated with habituation deficits.Results
We identified >100 genes required for habituation learning. For 93 of these genes, a
SUBMITTER: Fenckova M
PROVIDER: S-EPMC7053436 | biostudies-literature | 2019 Aug
REPOSITORIES: biostudies-literature