Lipids Regulate Export of Lysosomal Enzymes from the Endoplasmic Reticulum

Lysosomal enzymes are synthesized in the Endoplasmic Reticulum (ER) and transported to lysosomes to execute their functions. Deficiencies in lysosomal enzymes or components of the lysosomal transport machinery result in lysosomal storage disorders. While mannose-6-phosphate mediated lysosomal enzymes sorting in the Golgi has been extensively characterized, the mechanisms governing their export from the ER remain elusive. Here, we show that de novo lipogenesis, a metabolic pathway responsible for fatty acid synthesis, regulates lysosomal enzyme transport. Inhibition of de novo lipogenesis leads to the retention of lysosomal enzymes within the ER. Mechanistically, fatty acid derived from de novo lipogenesis is used for Arf1 myristoylation. Myristoylated Arf1 promotes retrograde vesicle trafficking from the Golgi to the ER, thereby maintaining the homeostatic bidirectional flux required for efficient ER export of lysosomal enzymes. Our findings uncover a critical functional link between lipid metabolism and lysosomal enzyme trafficking.

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Publication Details

Journal
bioRxiv (Cold Spring Harbor Laboratory)
Published
2026-04-17
DOI
https://doi.org/10.64898/2026.04.16.719038
Primary Topic
Calcium signaling and nucleotide metabolism
Type
article
Field-Weighted Citation Impact
0.00

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article

Lipids Regulate Export of Lysosomal Enzymes from the Endoplasmic Reticulum

Myeonghoon Han, Norbert Perrimon, I Park, Baolong Xia
bioRxiv (Cold Spring Harbor Laboratory)
Calcium signaling and nucleotide metabolism
article

Lipids Regulate Export of Lysosomal Enzymes from the Endoplasmic Reticulum

Myeonghoon Han, Norbert Perrimon, I Park, Baolong Xia
article en

Abstract

Lysosomal enzymes are synthesized in the Endoplasmic Reticulum (ER) and transported to lysosomes to execute their functions. Deficiencies in lysosomal enzymes or components of the lysosomal transport machinery result in lysosomal storage disorders. While mannose-6-phosphate mediated lysosomal enzymes sorting in the Golgi has been extensively characterized, the mechanisms governing their export from the ER remain elusive. Here, we show that de novo lipogenesis, a metabolic pathway responsible for fatty acid synthesis, regulates lysosomal enzyme transport. Inhibition of de novo lipogenesis leads to the retention of lysosomal enzymes within the ER. Mechanistically, fatty acid derived from de novo lipogenesis is used for Arf1 myristoylation. Myristoylated Arf1 promotes retrograde vesicle trafficking from the Golgi to the ER, thereby maintaining the homeostatic bidirectional flux required for efficient ER export of lysosomal enzymes. Our findings uncover a critical functional link between lipid metabolism and lysosomal enzyme trafficking.

bioRxiv (Cold Spring Harbor Laboratory)
Howard Hughes Medical Institute (US), Harvard University (US), Boston VA Research Institute (US)
Howard Hughes Medical Institute, Beth Israel Deaconess Medical Center, National Institutes of Health, National Institute of Arthritis and Musculoskeletal and Skin Diseases
Openalex Percentile: Top 20%
Calcium signaling and nucleotide metabolism
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