Wen Jianzhong, Xiao Junyu, Rahdar Meghdad, Choudhury Biswa P, Cui Jixin, Taylor Gregory S, Esko Jeffrey D, Dixon Jack E
Departments of Pharmacology and.
Cellular and Molecular Medicine, and.
Proc Natl Acad Sci U S A. 2014 Nov 4;111(44):15723-8. doi: 10.1073/pnas.1417993111. Epub 2014 Oct 20.
Most eukaryotic cells elaborate several proteoglycans critical for transmitting biochemical signals into and between cells. However, the regulation of proteoglycan biosynthesis is not completely understood. We show that the atypical secretory kinase family with sequence similarity 20, member B (Fam20B) phosphorylates the initiating xylose residue in the proteoglycan tetrasaccharide linkage region, and that this event functions as a molecular switch to regulate subsequent glycosaminoglycan assembly. Proteoglycans from FAM20B knockout cells contain a truncated tetrasaccharide linkage region consisting of a disaccharide capped with sialic acid (Siaα2-3Galβ1-4Xylβ1) that cannot be further elongated. We also show that the activity of galactosyl transferase II (GalT-II, B3GalT6), a key enzyme in the biosynthesis of the tetrasaccharide linkage region, is dramatically increased by Fam20B-dependent xylose phosphorylation. Inactivating mutations in the GALT-II gene (B3GALT6) associated with Ehlers-Danlos syndrome cause proteoglycan maturation defects similar to FAM20B deletion. Collectively, our findings suggest that GalT-II function is impaired by loss of Fam20B-dependent xylose phosphorylation and reveal a previously unappreciated mechanism for regulation of proteoglycan biosynthesis.
大多数真核细胞会合成多种蛋白聚糖,这些蛋白聚糖对于将生化信号传递到细胞内以及在细胞间传递至关重要。然而,蛋白聚糖生物合成的调控机制尚未完全明晰。我们发现,序列相似性20成员B(Fam20B)所属的非典型分泌激酶家族可使蛋白聚糖四糖连接区域中的起始木糖残基磷酸化,且这一过程充当分子开关,以调控后续糖胺聚糖的组装。来自FAM20B基因敲除细胞的蛋白聚糖含有一个截短的四糖连接区域,该区域由一个被唾液酸(Siaα2-3Galβ1-4Xylβ1)封端的二糖组成,无法进一步延长。我们还表明,半乳糖基转移酶II(GalT-II,B3GalT6)是四糖连接区域生物合成中的关键酶,其活性因Fam20B依赖的木糖磷酸化而显著增强。与埃勒斯-当洛综合征相关的GALT-II基因(B3GALT6)失活突变会导致与FAM20B缺失类似的蛋白聚糖成熟缺陷。总体而言,我们的研究结果表明,Fam20B依赖的木糖磷酸化缺失会损害GalT-II的功能,并揭示了一种此前未被认识的蛋白聚糖生物合成调控机制。