Key points are not available for this paper at this time.
Significance Approximately 1 in 100 people have epilepsy, and nearly 3% of epileptics have photosensitive epilepsy, which results in serious debilitating seizures. Despite these numbers, in 100 y of research, no clear single gene defect has been shown to be causative in photosensitive epilepsy in genetic models. Although sphingolipid defects have been shown to be causative for many lysosomal storage diseases in humans as well as animal models, our study shows an important connection to a neuronal disease, photosensitive epilepsy, using the fly system as a model. We show that in a Drosophila ceramide phosphoethanolamine synthase-null mutant cortical glial cells fail to establish plasma membrane processes required to encapsulate neuronal cell bodies, resulting in photosensitive epilepsy.
Turner‐Evans et al. (2018) studied this question.