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N -Glycan on the Non-Consensus N-X-C Glycosylation Site Impacts Activity, Stability, and Localization of the Sd a Synthase B4GALNT2

Title: N -Glycan on the Non-Consensus N-X-C Glycosylation Site Impacts Activity, Stability, and Localization of the Sd a Synthase B4GALNT2
Authors: Virginie Cogez; Dorothée Vicogne; Céline Schulz; Lucie Portier; Giulia Venturi; Jérôme de Ruyck; Mathieu Decloquement; Marc F. Lensink; Guillaume Brysbaert; Fabio Dall’Olio; Sophie Groux-Degroote; Anne Harduin-Lepers
Source: International Journal of Molecular Sciences, Vol 24, Iss 4, p 4139 (2023)
Publisher Information: MDPI AG
Publication Year: 2023
Collection: Directory of Open Access Journals: DOAJ Articles
Subject Terms: B4GALNT2; dimer; glycosyltransferase; N -glycan; unusual N-X-C glycosylation site; Biology (General); QH301-705.5; Chemistry; QD1-999
Description: The Sd a carbohydrate epitope and its biosynthetic B4GALNT2 enzyme are expressed in the healthy colon and down-regulated to variable extents in colon cancer. The human B4GALNT2 gene drives the expression of a long and a short protein isoform (LF-B4GALNT2 and SF-B4GALNT2) sharing identical transmembrane and luminal domains. Both isoforms are trans-Golgi proteins and the LF-B4GALNT2 also localizes to post-Golgi vesicles thanks to its extended cytoplasmic tail. Control mechanisms underpinning Sd a and B4GALNT2 expression in the gastrointestinal tract are complex and not fully understood. This study reveals the existence of two unusual N -glycosylation sites in B4GALNT2 luminal domain. The first atypical N-X-C site is evolutionarily conserved and occupied by a complex-type N -glycan. We explored the influence of this N -glycan using site-directed mutagenesis and showed that each mutant had a slightly decreased expression level, impaired stability, and reduced enzyme activity. Furthermore, we observed that the mutant SF-B4GALNT2 was partially mislocalized in the endoplasmic reticulum, whereas the mutant LF-B4GALNT2 was still localized in the Golgi and post-Golgi vesicles. Lastly, we showed that the formation of homodimers was drastically impaired in the two mutated isoforms. An AlphaFold2 model of the LF-B4GALNT2 dimer with an N -glycan on each monomer corroborated these findings and suggested that N -glycosylation of each B4GALNT2 isoform controlled their biological activity.
Document Type: article in journal/newspaper
Language: English
Relation: https://www.mdpi.com/1422-0067/24/4/4139; https://doaj.org/toc/1661-6596; https://doaj.org/toc/1422-0067; https://doaj.org/article/718199075d484811b20971a1a49b3239
DOI: 10.3390/ijms24044139
Availability: https://doi.org/10.3390/ijms24044139; https://doaj.org/article/718199075d484811b20971a1a49b3239
Accession Number: edsbas.C0D46CDD
Database: BASE