ArticleThe Journal of biological chemistry2013
Analysis of Drosophila glucuronyl C5-epimerase: implications for developmental roles of heparan sulfate sulfation compensation and 2-O-sulfated glucuronic acid.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- In vivo activities of heparan sulfate differentially modified by NDSTs during development.Proteoglycan research · 2024Article
- Chondroitin sulfate is required for follicle epithelial integrity and organ shape maintenance in Drosophila.Development (Cambridge, England) · 2023Article
- Regulation of morphogen pathways by a Drosophila chondroitin sulfate proteoglycan Windpipe.Journal of cell science · 2023Article
- A dominant negative splice variant of the heparan sulfate biosynthesis enzyme NDST1 reduces heparan sulfate sulfation.Glycobiology · 2022Article
- Analyzing the Role of Heparan Sulfate Proteoglycans in Axon Guidance In Vivo in Zebrafish.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Article
- Glypicans and Heparan Sulfate in Synaptic Development, Neural Plasticity, and Neurological Disorders.Frontiers in neural circuits · 2021Review
- HS2ST1-dependent signaling pathways determine breast cancer cell viability, matrix interactions, and invasive behavior.Cancer science · 2020Article
- Chondroitin sulfate proteoglycan Windpipe modulates Hedgehog signaling inMolecular biology of the cell · 2020Article
- Anionic and zwitterionic moieties as widespread glycan modifications in non-vertebrates.Glycoconjugate journal · 2020Review
- Triglyceride-rich lipoprotein binding and uptake by heparan sulfate proteoglycan receptors in a CRISPR/Cas9 library of Hep3B mutants.Glycobiology · 2019Article
- Establishment and characterization of Drosophila cell lines mutant for heparan sulfate modifying enzymes.Glycobiology · 2019Article
- Heparan Sulfate Microarray Reveals That Heparan Sulfate-Protein Binding Exhibits Different Ligand Requirements.Journal of the American Chemical Society · 2017Article
- The "in and out" of glucosamine 6-O-sulfation: the 6th sense of heparan sulfate.Glycoconjugate journal · 2017Review
- Determinants of Glycosaminoglycan (GAG) Structure.Biomolecules · 2015Review
- Structural and functional study of D-glucuronyl C5-epimerase.The Journal of biological chemistry · 2015Article
- Analyzing the role of heparan sulfate proteoglycans in axon guidance in vivo in zebrafish.Methods in molecular biology (Clifton, N.J.) · 2015Article
- D-glucuronyl C5-epimerase cell type specifically affects angiogenesis pathway in different prostate cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Transcriptional Activity of Heparan Sulfate Biosynthetic Machinery is Specifically Impaired in Benign Prostate Hyperplasia and Prostate Cancer.Frontiers in oncology · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
During the biosynthesis of heparan sulfate (HS), glucuronyl C5-epimerase (Hsepi) catalyzes C5-epimerization of glucuronic acid (GlcA), converting it to iduronic acid (IdoA). Because HS 2-O-sulfotransferase (Hs2st) shows a strong substrate preference for IdoA over GlcA, C5-epimerization is required for normal HS sulfation. However, the physiological significance of C5-epimerization remains elusive. To understand the role of Hsepi in development, we isolated Drosophila Hsepi mutants. Homozygous mutants are viable and fertile with only minor morphological defects, including the formation of an ectopic crossvein in the wing, but they have a short lifespan. We propose that two mechanisms contribute to the mild phenotypes of Hsepi mutants: HS sulfation compensation and possible developmental roles of 2-O-sulfated GlcA (GlcA2S). HS disaccharide analysis showed that loss of Hsepi resulted in a significant impairment of 2-O-sulfation and induced compensatory increases in N- and 6-O-sulfation. Simultaneous block of Hsepi and HS 6-O-sulfotransferase (Hs6st) activity disrupted tracheoblast formation, a well established FGF-dependent process. This result suggests that the increase in 6-O-sulfation in Hsepi mutants is critical for the rescue of FGF signaling. We also found that the ectopic crossvein phenotype can be induced by expression of a mutant form of Hs2st with a strong substrate preference for GlcA-containing units, suggesting that this phenotype is associated with abnormal GlcA 2-O-sulfation. Finally, we show that Hsepi formed a complex with Hs2st and Hs6st in S2 cells, raising the possibility that this complex formation contributes to the close functional relationships between these enzymes.
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