N-glycosylation, is a key regulator of ER morphology and dynamics. We have integrated multi-omics data and super-resolution imaging to characterize the broad effect of EXT1 inactivation, including ER shape-dynamics-function relationships in mammalian cells. We have observed that, inactivating EXT1 induces cell enlargement and enhances metabolic switches such as protein secretion. In particular, suppressing EXT1 in mouse thymocytes causes developmental dysfunctions associated to ER network extension. Our findings suggest that EXT1 drives glycosylation reactions involving ER structural proteins and high-energy nucleotide sugars, which might also apply to other organelles. Competing Interest Statement The University of Liege filed a patent application relating to the use of cells knocked down for EXT1 expression in biopharmaceuticals production (European Patent Office - Priority filing referred as EP20158875). Footnotes * ↵24 Lead contact * https://data.mendeley.com/datasets/y3h34szx5z/1 * https://data.mendeley.com/datasets/2mfzds3mmv/1 * https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE138030...

Exostosin-1 Glycosyltransferase Regulates Endoplasmic Reticulum Architecture and Dynamics

10.1101/2020.09.02.275925