State Key Laboratory of Protein and Plant Gene Research, Peking University, Beijing, China; School of Life Sciences, Peking University, Beijing, China.
School of Life Sciences, Peking University, Beijing, China.
J Biol Chem. 2022 Mar;298(3):101702. doi: 10.1016/j.jbc.2022.101702. Epub 2022 Feb 9.
GlcNAc-1-phosphotransferase catalyzes the initial step in the formation of the mannose-6-phosphate tag that labels ∼60 lysosomal proteins for transport. Mutations in GlcNAc-1-phosphotransferase are known to cause lysosomal storage disorders such as mucolipidoses. However, the molecular mechanism of GlcNAc-1-phosphotransferase activity remains unclear. Mammalian GlcNAc-1-phosphotransferases are α2β2γ2 hexamers in which the core catalytic α- and β-subunits are derived from the GNPTAB (N-acetylglucosamine-1-phosphate transferase subunits alpha and beta) gene. Here, we present the cryo-electron microscopy structure of the Drosophila melanogaster GNPTAB homolog, DmGNPTAB. We identified four conserved regions located far apart in the sequence that fold into the catalytic domain, which exhibits structural similarity to that of the UDP-glucose glycoprotein glucosyltransferase. Comparison with UDP-glucose glycoprotein glucosyltransferase also revealed a putative donor substrate-binding site, and the functional requirements of critical residues in human GNPTAB were validated using GNPTAB-knockout cells. Finally, we show that DmGNPTAB forms a homodimer that is evolutionarily conserved and that perturbing the dimer interface undermines the maturation and activity of human GNPTAB. These results provide important insights into GlcNAc-1-phosphotransferase function and related diseases.
GlcNAc-1-磷酸转移酶催化甘露糖-6-磷酸标签形成的第一步,该标签标记了大约 60 种溶酶体蛋白进行运输。已知 GlcNAc-1-磷酸转移酶的突变会导致溶酶体贮积症,如黏脂贮积症。然而,GlcNAc-1-磷酸转移酶活性的分子机制仍不清楚。哺乳动物的 GlcNAc-1-磷酸转移酶是α2β2γ2 六聚体,其中核心催化的α-和β-亚基来自 GNPTAB(N-乙酰葡萄糖胺-1-磷酸转移酶亚基α和β)基因。在这里,我们展示了黑腹果蝇 GNPTAB 同源物 DmGNPTAB 的冷冻电镜结构。我们鉴定了四个在序列中相隔很远的保守区域,这些区域折叠成催化结构域,其结构与 UDP-葡萄糖糖蛋白葡萄糖基转移酶相似。与 UDP-葡萄糖糖蛋白葡萄糖基转移酶的比较还揭示了一个可能的供体底物结合位点,并使用 GNPTAB 敲除细胞验证了人类 GNPTAB 中关键残基的功能要求。最后,我们表明 DmGNPTAB 形成同源二聚体,该二聚体在进化上是保守的,并且扰乱二聚体界面会破坏人类 GNPTAB 的成熟和活性。这些结果为 GlcNAc-1-磷酸转移酶功能和相关疾病提供了重要的见解。