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- W4285385627 abstract "Recessive variants in GBA1 cause Gaucher disease, a prevalent form of lysosome storage disease. GBA1 encodes a lysosomal enzyme that hydrolyzes glucosylceramide (GlcCer) into glucose and ceramide. Its loss causes lysosomal dysfunction and increased levels of GlcCer. We generated a null allele of the Drosophila ortholog Gba1b by inserting the Gal4 using CRISPR-Cas9. Here, we show that Gba1b is expressed in glia but not in neurons. Glial-specific knockdown recapitulates the defects found in Gba1b mutants, and these can be rescued by glial expression of human GBA1 . We show that GlcCer is synthesized upon neuronal activity, and it is transported from neurons to glia through exosomes. Furthermore, we found that glial TGF-β/BMP induces the transfer of GlcCer from neurons to glia and that the White protein, an ABCG transporter, promotes GlcCer trafficking to glial lysosomes for degradation." @default.
- W4285385627 created "2022-07-14" @default.
- W4285385627 creator A5001856843 @default.
- W4285385627 creator A5001965184 @default.
- W4285385627 creator A5024407328 @default.
- W4285385627 creator A5026995692 @default.
- W4285385627 creator A5052297489 @default.
- W4285385627 creator A5073407564 @default.
- W4285385627 creator A5085561212 @default.
- W4285385627 date "2022-07-15" @default.
- W4285385627 modified "2023-10-16" @default.
- W4285385627 title "Neuronal activity induces glucosylceramide that is secreted via exosomes for lysosomal degradation in glia" @default.
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