Faculty and Student Publications

Document Type

Article

Publication Date

11-30-2021

Abstract

Drosophila’s white gene encodes an ATP binding cassette G-subfamily (ABCG) half transporter. White is closely related to mammalian ABCG family members that function in cholesterol efflux. Mutants of white have several behavioral phenotypes that are independent of visual defects. This study characterizes a novel defect of white mutants in the acquisition of olfactory memory using the aversive olfactory conditioning paradigm. The w1118 mutants learned slower than wildtype controls, yet with additional training, they reached wildtype levels of performance. The w1118 learning phenotype is also found in the wapricot and wcoral alleles, is dominant, and is rescued by genomic white and mini-white transgenes. Reducing dietary cholesterol strongly impairs olfactory learning for wildtype controls, while w1118 mutants are resistant to this deficit. The w1118 mutants display higher levels of cholesterol and cholesterol esters than wildtype under this low cholesterol diet. Increasing serotonin and/or dopamine levels in the white mutants significantly improved w1118 learning. However, serotonin levels were not lower in the heads of the w1118 mutants than in wildtype controls. There were also no significant differences found in synapse numbers within the w1118 brain. We propose that the w1118 learning defect may be due to inefficient biogenic amine signaling brought about by altered cholesterol homeostasis.

Relational Format

journal article

Comments

Additional file: Data set to accompany article

DOI

https://doi.org/10.3390/ijms222312967

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