Department of Biochemistry, Kobe Pharmaceutical University, Higashinada-ku, Kobe 658-8558, Japan.
Department of Biochemistry, Kobe Pharmaceutical University, Higashinada-ku, Kobe 658-8558, Japan.
J Biol Chem. 2014 Mar 7;289(10):6695-6708. doi: 10.1074/jbc.M113.520536. Epub 2014 Jan 14.
Recently, we demonstrated that FAM20B is a kinase that phosphorylates the xylose (Xyl) residue in the glycosaminoglycan-protein linkage region of proteoglycans. The phosphorylation of Xyl residues by FAM20B enhances the formation of the linkage region. Rapid dephosphorylation is probably induced just after synthesis of the linker and just before polymerization initiates. Indeed, in vitro chondroitin or heparan sulfate polymerization does not occur when the Xyl residue of the tetrasaccharide linkage region is phosphorylated. However, the enzyme responsible for the dephosphorylation of Xyl remains unknown. Here, we identified a novel protein that dephosphorylates the Xyl residue and designated it 2-phosphoxylose phosphatase. The phosphatase efficiently removed the phosphate from the phosphorylated trisaccharide, Galβ1-3Galβ1-4Xyl(2-O-phosphate), but not from phosphorylated tetrasaccharide, GlcUAβ1-3Galβ1-3Galβ1-4Xyl(2-O-phosphate). Additionally, RNA interference-mediated inhibition of 2-phosphoxylose phosphatase resulted in increased amounts of GlcNAcα1-4GlcUAβ1-3Galβ1-3Galβ1-4Xyl(2-O-phosphate), Galβ1-3Galβ1-4Xyl(2-O-phosphate), and Galβ1-4Xyl(2-O-phosphate) in the cells. Gel filtration analysis of the glycosaminoglycan chains synthesized in the knockdown cells revealed that these cells produced decreased amounts of glycosaminoglycan chains and that the chains had similar lengths to those in the mock-transfected cells. Transcripts encoding this phosphatase were ubiquitously, but differentially, expressed in human tissues. Moreover, the phosphatase localized to the Golgi and interacted with the glucuronyltransferase-I involved in the completion of the glycosaminoglycan-protein linkage region. Based on these findings, we conclude that transient phosphorylation of the Xyl residue in the glycosaminoglycan-protein linkage region controls the formation of glycosaminoglycan chains of proteoglycans.
最近,我们证明 FAM20B 是一种激酶,可使蛋白聚糖糖胺聚糖-蛋白连接区域中的木糖(Xyl)残基发生磷酸化。FAM20B 对 Xyl 残基的磷酸化增强了连接区域的形成。在合成连接子后和聚合开始前,磷酸化可能会迅速去磷酸化。事实上,当四糖连接区域的 Xyl 残基发生磷酸化时,软骨素或硫酸乙酰肝素聚合不会发生。但是,负责 Xyl 去磷酸化的酶仍然未知。在这里,我们鉴定了一种可使 Xyl 残基去磷酸化的新型蛋白,并将其命名为 2-磷酸木酮糖磷酸酶。该磷酸酶可有效地从磷酸化的三糖中去除磷酸,Galβ1-3Galβ1-4Xyl(2-O-磷酸),但不能从磷酸化的四糖中去除,GlcUAβ1-3Galβ1-3Galβ1-4Xyl(2-O-磷酸)。此外,RNA 干扰介导的 2-磷酸木酮糖磷酸酶抑制导致细胞中 GlcNAcα1-4GlcUAβ1-3Galβ1-3Galβ1-4Xyl(2-O-磷酸)、Galβ1-3Galβ1-4Xyl(2-O-磷酸)和 Galβ1-4Xyl(2-O-磷酸)的含量增加。对敲低细胞中合成的糖胺聚糖链进行凝胶过滤分析表明,这些细胞产生的糖胺聚糖链减少,并且这些链的长度与mock 转染细胞中的相似。该磷酸酶的编码转录本在人类组织中广泛但不同地表达。此外,该磷酸酶定位于高尔基体并与参与糖胺聚糖-蛋白连接区域完成的葡萄糖醛酸基转移酶-I 相互作用。基于这些发现,我们得出结论,糖胺聚糖-蛋白连接区域中 Xyl 残基的短暂磷酸化控制了蛋白聚糖糖胺聚糖链的形成。