ArticleThe Journal of biological chemistry2012
The Drosophila neurally altered carbohydrate mutant has a defective Golgi GDP-fucose transporter.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Review
- A new nodavirus-negative Trichoplusia ni cell line for baculovirus-mediated protein production.Biotechnology and bioengineering · 2020Article
- Structures and functions of invertebrate glycosylation.Open biology · 2019Review
- Characterization of a GDP-Fucose Transporter and a Fucosyltransferase Involved in the Fucosylation of Glycoproteins in the DiatomFrontiers in plant science · 2019Article
- Modeling Congenital Disorders of N-Linked Glycoprotein Glycosylation inFrontiers in genetics · 2018Review
- The fucomic potential of mosquitoes: Fucosylated N-glycan epitopes and their cognate fucosyltransferases.Insect biochemistry and molecular biology · 2016Article
- Phenotype-based clustering of glycosylation-related genes by RNAi-mediated gene silencing.Genes to cells : devoted to molecular & cellular mechanisms · 2015Article
- Negative feedback regulation of Wnt signaling via N-linked fucosylation in zebrafish.Developmental biology · 2014Article
- Understanding human glycosylation disorders: biochemistry leads the charge.The Journal of biological chemistry · 2013Review
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Authors and funding
8 authors.
Funding
Abstract
Studying genetic disorders in model organisms can provide insights into heritable human diseases. The Drosophila neurally altered carbohydrate (nac) mutant is deficient for neural expression of the HRP epitope, which consists of N-glycans with core α1,3-linked fucose residues. Here, we show that a conserved serine residue in the Golgi GDP-fucose transporter (GFR) is substituted by leucine in nac(1) flies, which abolishes GDP-fucose transport in vivo and in vitro. This loss of function is due to a biochemical defect, not to destabilization or mistargeting of the mutant GFR protein. Mass spectrometry and HPLC analysis showed that nac(1) mutants lack not only core α1,3-linked, but also core α1,6-linked fucose residues on their N-glycans. Thus, the nac(1) Gfr mutation produces a previously unrecognized general defect in N-glycan core fucosylation. Transgenic expression of a wild-type Gfr gene restored the HRP epitope in neural tissues, directly demonstrating that the Gfr mutation is solely responsible for the neural HRP epitope deficiency in the nac(1) mutant. These results validate the Drosophila nac(1) mutant as a model for the human congenital disorder of glycosylation, CDG-IIc (also known as LAD-II), which is also the result of a GFR deficiency.
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