ArticleThe Journal of biological chemistry2013
The role of Drosophila heparan sulfate 6-O-endosulfatase in sulfation compensation.
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 9 papers.
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Who cites it
9 citing papers in PubMed.
- Review
- In vivo activities of heparan sulfate differentially modified by NDSTs during development.Proteoglycan research · 2024Article
- Regulation of morphogen pathways by a Drosophila chondroitin sulfate proteoglycan Windpipe.Journal of cell science · 2023Article
- Establishment and characterization of Drosophila cell lines mutant for heparan sulfate modifying enzymes.Glycobiology · 2019Article
- Loss of heparan sulfate in the niche leads to tumor-like germ cell growth in the Drosophila testis.Glycobiology · 2018Article
- Deciphering functional glycosaminoglycan motifs in development.Current opinion in structural biology · 2018Review
- Heparan sulfate regulates the number and centrosome positioning of Drosophila male germline stem cells.Molecular biology of the cell · 2016Article
- Selective binding of C-6 OH sulfated hyaluronic acid to the angiogenic isoform of VEGF(165).Biomaterials · 2016Article
- Analysis of Drosophila glucuronyl C5-epimerase: implications for developmental roles of heparan sulfate sulfation compensation and 2-O-sulfated glucuronic acid.The Journal of biological chemistry · 2013Article
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Authors and funding
7 authors.
Funding
Abstract
The biosynthesis of heparan sulfate proteoglycans is tightly regulated by multiple feedback mechanisms, which support robust developmental systems. One of the regulatory network systems controlling heparan sulfate (HS) biosynthesis is sulfation compensation. A previous study using Drosophila HS 2-O- and 6-O-sulfotransferase (Hs2st and Hs6st) mutants showed that loss of sulfation at one position is compensated by increased sulfation at other positions, supporting normal FGF signaling. Here, we show that HS sulfation compensation rescues both Decapentaplegic and Wingless signaling, suggesting a universal role of this regulatory system in multiple pathways in Drosophila. Furthermore, we identified Sulf1, extracellular HS 6-O-endosulfatase, as a novel component of HS sulfation compensation. Simultaneous loss of Hs2st and Sulf1 led to 6-O-oversulfation, leading to patterning defects, overgrowth, and lethality. These phenotypes are caused at least partly by abnormal up-regulation of Hedgehog signaling. Thus, sulfation compensation depends on the coordinated activities of Hs2st, Hs6st, and Sulf1.
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Registered trials
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